The Vaccine Damage Science

THE CENTRAL ROLE OF IMMUNOEXCITOTOXICITY IN ALUMINUM AND MERCURY-CONTAINING ADJUVANT-TRIGGERED NEURODEVELOPMENTAL AND NEURODEGENERATIVE DISORDERS Dr. Russell Blaylock is a board certified neurosurgeon, author and lecturer. He attended the Louisiana State University School of Medicine in New Orleans and completed his general surgical internship and neurosurgical residency at the Medical University of South Carolina in Charleston, South Carolina. During his residency training he worked with the eminent neurosurgeon, Dr. Ludwig Kempe. Together they developed the transcallosal removal of intraventricular tumors, a technique still used today. For the past 25 years he has practiced neurosurgery in addition to having a nutritional practice. He recently retired from his neurosurgical duties to devote his full attention to nutritional studies and neuroscience research.https://www.youtube.com/watch?v=u9DkcpEEBPI (the same video as above, Session 22) Published Papers – Dr. Russell Blaylockhttp://www.russellblaylockmd.com/ Neurosurgeon issues public challenge to vaccine zealots: Inject yourselves with all shots you say children should get!http://www.naturalnews.com/035335_vaccines_Dr_Blaylock_children.html Dr. Russell Blaylock interview on mandatory vaccine trials, fraudulent vaccine science, and vaccine ethics - March 2012http://tv.naturalnews.com/v.asp?v=DFBE7C32CBDBF43B7342333B7D827EB0 Dr. Russell Blaylock exposes the criminal fraud of Gardasil, HPV vaccinationshttp://www.naturalnews.com/036874_Dr_Russell_Blaylock_Gardasil_HPV_vaccines.html

This below is a newly emerging information and worth consideration in the environmental/vaccine causation of ASD. Obviously any child with this situation existing, would likely not be able to detoxify vaccines, nor multiple vaccines. This condition no appears to be far more prevalent than anyone has previously known.

MTHFR-Genetics, Autism, and Disease

MTHFR stands for MethylTetraHydroFolate Reductase Deficiency. MTHFR is a genetic disorder that inhibits some people from being able to convert folic acid from food to the active form of folic acid, L-methylfolate, that is used by the body. MTHFR was identified in the Human Genome Project, a study designed to identify treatable genetic disorders.

http://www.vacfacts.info/mthfr-genetics-autism-and-disease.html This listing takes a look at some of the unbiased selections of vaccine science that show an entirely different story than the vaccines are safe and effective jargon that we are typically told. This selection explores the propaganda filled myths and as well the vaccine related misinformation we have repeatedly been fed.

Pediatr Infect Dis. 1983 Jan-Feb;2(1):7-11. Possible temporal association between diphtheria-tetanus toxoid-pertussis vaccination and sudden infant death syndrome. Baraff LJ, Ablon WJ, Weiss RC. http://www.ncbi.nlm.nih.gov/pubmed/6835859 Newly published research by Keele Conference scientists shows that aluminum adjuvant in vaccines transfers to the brain. They have documented the path from injection site to the brain, and that once in the brain, it persists. Newborns, the elderly, and people with a certain genetic variation are particularly at risk.

Long-term biodistribution of nanomaterials used in medicine is largely unknown. This is the case for alum, the most widely used vaccine adjuvant, which is a nanocrystalline compound spontaneously forming micron/submicron-sized agglomerates. Although generally well tolerated, alum is occasionally detected within monocyte-lineage cells long after immunization in presumably susceptible individuals with systemic/neurologic manifestations or autoimmune (inflammatory) syndrome induced by adjuvants (ASIA).

Methods

On the grounds of preliminary investigations in 252 patients with alum-associated ASIA showing both a selective increase of circulating CCL2, the major monocyte chemoattractant, and a variation in the CCL2 gene, we designed mouse experiments to assess biodistribution of vaccine-derived aluminum and of alum-particle fluorescent surrogates injected in muscle. Aluminum was detected in tissues by Morin stain and particle induced X-ray emission) (PIXE) Both 500 nm fluorescent latex beads and vaccine alum agglomerates-sized nanohybrids (Al-Rho) were used.

Results

Intramuscular injection of alum-containing vaccine was associated with the appearance of aluminum deposits in distant organs, such as spleen and brain where they were still detected one year after injection. Both fluorescent materials injected into muscle translocated to draining lymph nodes (DLNs) and thereafter were detected associated with phagocytes in blood and spleen. Particles linearly accumulated in the brain up to the six-month endpoint; they were first found in perivascular CD11b+ cells and then in microglia and other neural cells. DLN ablation dramatically reduced the biodistribution. Cerebral translocation was not observed after direct intravenous injection, but significantly increased in mice with chronically altered blood-brain-barrier. Loss/gain-of-function experiments consistently implicated CCL2 in systemic diffusion of Al-Rho particles captured by monocyte-lineage cells and in their subsequent neurodelivery. Stereotactic particle injection pointed out brain retention as a factor of progressive particle accumulation.

Conclusion

Nanomaterials can be transported by monocyte-lineage cells to DLNs, blood and spleen, and, similarly to HIV, may use CCL2-dependent mechanisms to penetrate the brain. This occurs at a very low rate in normal conditions explaining good overall tolerance of alum despite its strong neurotoxic potential. However, continuously escalating doses of this poorly biodegradable adjuvant in the population may become insidiously unsafe, especially in the case of overimmunization or immature/altered blood brain barrier or high constitutive CCL-2 production.

Source: Department of Economics and Finance, Baruch College/City University of New York, New York, New York, USA.

Abstract

The reason for the rapid rise of autism in the United States that began in the 1990s is a mystery. Although individuals probably have a genetic predisposition to develop autism, researchers suspect that one or more environmental triggers are also needed. One of those triggers might be the battery of vaccinations that young children receive. Using regression analysis and controlling for family income and ethnicity, the relationship between the proportion of children who received the recommended vaccines by age 2 years and the prevalence of autism (AUT) or speech or language impairment (SLI) in each U.S. state from 2001 and 2007 was determined. A positive and statistically significant relationship was found: The higher the proportion of children receiving recommended vaccinations, the higher was the prevalence of AUT or SLI. A 1% increase in vaccination was associated with an additional 680 children having AUT or SLI. Neither parental behavior nor access to care affected the results, since vaccination proportions were not significantly related (statistically) to any other disability or to the number of pediatricians in a U.S. state. The results suggest that although mercury has been removed from many vaccines, other culprits may link vaccines to autism. Further study into the relationship between vaccines and autism is warranted.

One of the first arguments people make when they are introduced to the idea that vaccines could be causing harm and/or ASD is that isn’t so, thus claiming as the CDC does, that the science shows there is no link. Really; well when all of the science they are showing you is only that cherry picked by the sources which to much to lose if the vaccine truth be known, then quite obviously you can realize that they are not going to consider any available science that doesn’t support their safe and effective agenda. And of course, that is exactly what they have done. In fact ta the federal vaccine court, the studies they accept carrying the most decision weight, have been only those funded by the CDC, on one single vaccine MMR, and one single vaccine ingredient, Thimerosal. No studies on multiple repeat vaccines, none on the safety of aluminum adjuvants, and of course no mention is ever made of obviously existing and potential vaccine contamination, known and unknown.

THE GREATER GOOD Team fully agrees with this premise. This compilation of research contains over 180 papers published in peer reviewed medical and scientific journals that explore and discuss injuries linked to vaccines. We have compiled this catalogue of science to help parents, lawmakers, medical practitioners and scientists understand several important points about the vaccine issue:

• there is abundant science published in mainstream medical and scientific journals suggesting cause for concern about the safety of vaccines;

• the vaccine debate is not a debate between parents and doctors but rather amongst scientists with opposing views;

• vaccines may be linked to a host of chronic illnesses and conditions such as asthma, allergies, learning disabilities, behavioral problems, autism, unexplained infant death and autoimmune diseases such as diabetes, rheumatoid arthritis, lupus, MS, and others;

• there are connections between the gut, immune, and neurological issues often seen in vaccine injuries.

This compilation does not contain all the science on vaccines but rather the science that suggests cause for concern. Readers should understand that the research cited here does not prove all the conditions mentioned are caused by vaccines. Rather, this research demonstrates that vaccine safety concerns are valid and warrant further investigation to fully evaluate the true long-term impact of vaccination.

To use this resource, simply browse all the different categories to familiarize yourself with the scope and breadth of the possible adverse reactions to vaccines.

You can't take anything at face value...especially when profit is involved. Ginger Taylor said it best:

"This report falls under the category of garbage in - garbage out.

#1. This was a "study" not the gold standard, double-blind placebo research.#2. True, previous studies have "not specifically considered autism"#3. This study only looked at the antigens in vaccines (that part of "germs" that the body responds to) and NEVER even looked at the other ingredients in vaccines, especially the adjuvants...the additives in vaccines used to get the body to have an extreme reaction.#4. The study never looked at the total number of vaccines children are injected with and gave no consideration to vaccine combinations.#5. The study looked at only about 1,000 children...all of them vaccinated. Where is the study of vaxed/un-vaxed children?? The CDC does NOT want parents to see that evidence.#6. "Kids are exposed to viruses in the same way as vaccines"??? You've got to be kidding!! Natural pathogens enter the body through inhalation or ingestion. Vaccines enter the body through injection. This is NOT exposure in the same way at all.#7. My favorite lie of all time, "it's been estimated that kids could theoretically receive THOUSANDS of vaccines at once". Go ahead vaccine pushers...you first."

Abstract: This paper makes two claims: (1) autism can be characterized as a chronic lowgrade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is provoked by a systemic deficiency in sulfate, but associated seizures and fever support sulfate restoration. We argue that impaired synthesis of cholesterol sulfate in the skin and red blood cells, catalyzed by sunlight and nitric oxide synthase enzymes, creates a state of colloidal instability in the

blood manifested as a low zeta potential and increased interfacial stress. Encephalitis, while life-threatening, can result in partial renewal of sulfate supply, promoting neuronal survival. Research is cited showing how taurine may not only help protect neurons from hypochlorite exposure, but also provide a source for sulfate renewal. Several environmental factors can synergistically promote the encephalopathy of autism, including the herbicide, glyphosate, aluminum, mercury, lead, nutritional deficiencies in thiamine and zinc, and yeast overgrowth due to excess dietary sugar. Given these facts, dietary and lifestyle changes, including increased sulfur ingestion, organic whole foods, increased sun exposure, and avoidance of toxins such as aluminum, mercury, and lead, may help to alleviate symptoms or, in some instances, to prevent autism altogether.

Stephanie Seneff is a Senior Research Scientist at the MIT Computer Science and Artificial Intelligence Laboratory. She received the B.S. degree in Biophysics in 1968, the M.S. and E.E. degrees in Electrical Engineering in 1980, and the Ph.D degree in Electrical Engineering and Computer Science in 1985, all from MIT. For over three decades, her research interests have always been at the intersection of biology and computation â€“ developing a computational model for the human auditory system, understanding human language so as to develop algorithms and systems for human computer interactions, as well as applying natural language processing (NLP) techniques to gene predictions. She has published over 170 refereed articles on these subjects, and has been invited to give keynote speeches at several international conferences. She has also supervised numerous Master's and PhD theses at MIT. In 2012, Dr. Seneff was elected Fellow of the International Speech and Communication Association (ISCA).

In recent years, Dr. Seneff has focused her research interests back towards biology. She is concentrating mainly on the relationship between nutrition and health. Since 2011, she has written 10 papers (7 as first author) in various medical and health-related journals on topics such as modern day diseases (e.g., Alzheimer, autism, cardiovascular diseases), analysis and search of databases of drug side effects using NLP techniques, and the impact of nutritional deficiencies and environmental toxins on human health. (more studies)

Aluminum toxicity is a widespread problem in all forms of life, including humans, animals, fish, plants and trees, and causes widespread degradation of the environment and health. Over 7000 reference articles on aluminum toxicity exist in various data bases; ( as of 1996 ) all recognizing the toxicity but concluding the mechanism of action is unknown. — [ Search results - scirus.com ]

Despite the number of references to aluminum toxicity, the FDA has always exempted it from testing from testing by putting it on their "Generally Regarded as Safe" ( GRAS ) list. Aluminum can be added to foods, medicines or water without restriction from the FDA.

[ Aluminum is known to stop cell division during the "S Phase", at levels less than 4 ppm. ]

The mechanism of action of aluminum toxicity is aluminum’s effect on carrying capacity or Zeta Potential. Aluminum is relatively non-toxic in and of itself. However, it destroys the carrying capacity of a liquid.

Aluminum has three ( 3 ) positive ions, so a single ion of aluminum will reduce surface charge, reduce carrying capacity and increase surface tension by 6,000 times the amount that an ion of Sodium, which has one ( 1 ) positive charge, would.

From: History of crime against the Food Laws (1929) by Dr. Riley, the prime mover behind the original Pure Food Law and Director of the FDA. He resigned in disgust in 1912 over exceptions granted to the law and lack of enforcement.

Aluminum has been exempted from testing for safety by the FDA under a convoluted logic wherein it is classified as GRAS. (Generally Regarded As Safe.) It has never been tested by the FDA on its safety and there are NO restrictions whatever on the amount or use of aluminum. Diseases Associated with Aluminium Intoxication. H. Tomlinson, M.B., Ch.B., MRCS., LRCP. Since that time thousands of studies have been published indicating aluminum is involved in neurological dysfunction, immunocompetence, as well as a host of other morbidities. I cannot begin to reference them all. Sepsis: a cause of aluminum release from tissue stores associated with acute neurological dysfunction and mortality. Davenport A. – Williams P.S. – Roberts N.B. – Bone J.M. From: Clin Nephrol (1988 Jul) 30(1):48-51.

We report six cases of patients with renal failure and exposure to aluminum who developed septicemia. In all cases the serum aluminum increased markedly. This may have contributed to the neurological dysfunction seen in five, and the deaths of four of the patients. We suggest that the rise in serum aluminum was due to the release of tissue-bound aluminum, resulting in an increase in free, diffusible aluminum and that this jeopardized both neurological function and immunocompetence.

Note that a lot of processed foods with chemical preservatives, pesticide residue and additives are of a cationic 1:1, 2:1 nature. Bad for humans. These foods have a natural zeta potential lowering effect on the blood.

From a file of 1127 children in whom signs of brain damage were reported after injections of vaccines containing pertussis antigen, the first 197 cases with good documentation of events were chosen for further study. In these children, 291 reactions had been reported, usually of screaming attacks (68), convulsions (87), collapse (17), or one or more of these signs (99), within 24 hours of injection. Subsequently 165 children became mentally defective and 102 had further convulsions. In 129 (65%), contraindications to vaccination were present ab initio and in 25, subsequent injections were given despite reactions to a previous injection or injections.

From a mathematical model constructed from data in published reports, it is calculated that the frequency of convulsions appears to be higher by 2: 1 in vaccinated than in unvaccinated infants. In children subject to febrile or other convulsions, the frequencies may be of the same order but a second convulsion occurring only after a second or subsequent injection of vaccine is unlikely to be due to chance.

The pattern of reactions and sequence of events observed in the present study and in published reports suggest an association between certain reactions to pertussis vaccine and subsequent severe brain damage, the incidence of which appears to be not less than one per fifty thousand children vaccinated during the last 20 years of mass vaccination in the United Kingdom.

I believe as to the above study, that in reality that said 1 in 50,000 is actually a very incorrect estimate. It is much more common than that. Standard DPT was damaging and killing infants and children on a regular basis thus was the reason they enacted the law and started the federal vaccine court. Although the DTaP vaccine, etc is of course less reactive being a non live vaccine, does NOT mean it is not doing the same thing on a lessor scale. By any means that number is obviously far more than just 1 in 50,000.

The pattern of reactions and sequence of events observed in the present study and in published reports suggest an association between certain reactions to pertussis vaccine and subsequent severe brain damage, the incidence of which appears to be not less than one per fifty thousand children vaccinated during the last 20 years of mass vaccination in the United Kingdom.

Metal pollutants are a global health risk due to their ability to contribute to a variety of diseases. Aluminum (Al), a ubiquitous environmental contaminant is implicated in anemia, osteomalacia, hepatic disorder, and neurological disorder. In this review, we outline how this intracellular generator of reactive oxygen species (ROS) triggers a metabolic shift towards lipogenesis in astrocytes and hepatocytes. This Al-evoked phenomenon is coupled to diminished mitochondrial activity, anerobiosis, and the channeling of α-ketoacids towards anti-oxidant defense. The resulting metabolic reconfiguration leads to fat accumulation and a reduction in ATP synthesis, characteristics that are common to numerous medical disorders. Hence, the ability of Al toxicity to create an oxidative environment promotes dysfunctional metabolic processes in astrocytes and hepatocytes. These molecular events triggered by Al-induced ROS production are the potential mediators of brain and liver disorders.

Aluminum Adjuvants - Lack of Safety Data - Lack of Aluminum Adjuvant Safety Studies, ( there are zero existing vaccine safety studies on aluminum adjuvants at the CDC and as well AS EVER EXISTED on the Paul Offit, CHOP site).http://www.vacfacts.info/aluminum-vaccine-adjuvants.html

Aluminum Adjuvant in Vaccines Causes Risk to Children According to New Journal Report

A new Canadian study of the mechanisms of aluminum adjuvant toxicity in pediatric patients confirms that immune challenges during early development, including those vaccine-induced, can lead to permanent detrimental alterations of the brain and immune system function. Lucija Tomljenovic, PhD and Christopher A. Shaw, PhD of the University of British Columbia’s evidence-based study was recently published in Lupus, the only fully peer reviewed international journal devoted exclusively to lupus (and related disease) research.

In addition to playing a major role in physiological immune responses against foreign antigens, the interleukin 2 (IL-2)-IL-2 receptor (IL-2R) system may also be implicated in autoimmune phenomena. Initial studies on the role of IL-2 in autoimmunity indicate a deficiency in the production of this lymphokine in autoimmune disease. Here, Guido Kroemer and Georg Wick review recent data supporting the notion that an excess of endogenous or exogenous IL-2 may aggravate autoaggression by triggering autoreactive effector cells, and they speculate that IL-2 might favor the de novo development of autoimmunity by breaking autotolerance.

Systemic autoimmunity appears to be the inevitable consequence of over-stimulating the host's immune ‘system’ by repeated immunization with antigen, to the levels that surpass system's self-organized criticality.

Now, when you review this next information, and if you were to know and to as well have investigated and understand what is actually in vaccines, then it becomes all to obvious how those vaccines and multiple repeat vaccines can cause the harm that they do. Then you add the real understanding of the means of and to physiological health, that has been hidden to mainstream so called medicine. (Thats right, I said hidden and as to as well the public); then in the bigger picture you can fully understand why vaccines are not worth the risk, nor in the true knowledge of what they have done to the health of our entire society. Think its not true, then you have not done the unbiased research that you will need to do. It is all up to you. You can chose to learn of and accept the truth, or you can remain mislead, and /or continue to deny the facts and the truth.

And if they want to deny where that brain inflammation is coming from in those found with it and having ASD, Pubmed is full of studies showing the inflammatory effect of aluminum adjuvants. That is how they work. Stimulating the immune system to go on high alert to actually recognized a killed/attenuated virus or bacterial pathogen in a vaccine. None of this, is rocket science! What else can adjuvants do? How about cause your immune system to become dysregulated and now be incorrectly recognizing self or organ cells as non self. How about allergens that the immune system was leaving alone; now it is picking that up to. Not in all, but just in some. How many? They will likely never know.

Now, you did not see them mention and causation nor vaccines, in the last Johns Hopkins study above; nor did they suggest any causation as to the cause of that said neuroinflammation in the brain. They instead only refer to it as inflammation syndromes. They in this study do not even suggest a cause, and as if they are clueless as to the cause. They have proven that this situation exists; so why are they not at least suggesting a causation?

However, many other studies we can find do show that this said repeat and chronic activation of the brains microgilia, is caused by aluminum adjuvants and thus the vaccines! That includes the published papers of Dr. Russell Blaylock, and studies a swell from several other sources. Sources that indeed are accepted and peer reviewed from real and substantial health care journals, but just not from a pharma connected journal. Neurology and toxicology related journals are the only place you will find them

Pubmed, and in fact several other publications all have pointed to aluminum adjuvants having the effect of an inflammatory response and resulting sensitization as to the physiological mechanisms of adjuvant effect on the immune system, such as so as as the immune system will then recognize the vaccine manufacturing created and so called killed or attenuated pathogen/antigen. Yet most of these study publications have as well repeated claimed that the action of an aluminum adjuvant, is not fully understood. Obviously they have not understood as well the over activation of the brains microglia, and resulting chronic brain inflammation, due to repeat and multiple vaccines containing an injected aluminum adjuvant.

Received 23 March 2005; received in revised form 19 April 2005; accepted 20 April 2005

Excerpt:

The promoters of genes up-regulated by aluminum are enriched in binding sites for the stress-inducible transcription factors HIF-1 and NF-kappaB, suggesting a role for aluminum, HIF-1 and NF-kappaB in driving atypical, pro-inflammatory and pro-apoptotic gene expression. The effect of aluminum on specific stress-related gene expression patterns in human brain cells clearly warrant further investigation.

When a child has an adverse reaction to vaccines, doctors and pediatricians tell parents to give the child Tylenol, correct? Tylenol can deplete glutathione, necessary for detoxification and as well detoxification of mercury, (Thimerosal), and also vaccine aluminum adjuvants. And what do they pediatricians and doctors not get about fever being necessary for the child to recover from pathogen created illness, even be it vaccine induced.

Effect of acetaminophen administration on hepatic glutathione compartmentation and mitochondrial energy metabolism in the rat.

Vendemiale G, Grattagliano I, Altomare E, Turturro N, Guerrieri F.

Source: Department of Internal Medicine, University of Bari, Italy.

Excerpt: Our findings suggest that acetaminophen administration selectively depletes (within 2 hr) mitochondrial glutathione, and produces local toxicity by altering membrane permeability and decreasing the efficiency of oxidative phosphorylation. This renders mitochondria more susceptible to oxidative damage, especially during increased free radical production, as in the case of enhanced mitochondrial respiration in State 4. The concomitant restoration of mitochondrial respiration, oxidative phosphorylation, membrane permeability, and glutathione levels is consistent with the importance of the mitochondrial glutathione pool for the protection of the mitochondrial membrane against oxidative damage.

Oh YES, we clearly have a huge problem, Houston!!! Can you see it? WE have been mislead and LIED to. We as well have CDC ground control still attempting to call for the vaccine science on literally the old wooden crank telephones, and everyone knows they are no longer working. The general public does not even realize that is being done deliberately. Oh, they will still say, these studies do not mention vaccines as causation, nor the vaccine aluminum adjuvants. Here is a clue, we AS WELL have the studies that do show the actual causation of that overactivation of the brains microlia cells and resulting chronic levels of brain inflammation, being the aluminum adjuvants, (combined with the antigen and as well vaccine contamination; look at as well the information on Gardasil)! Why did these studies find the over-activation of the brains microglia, and the inflammation, but never looked for nor even suggested a causation? As if they are oblivious to the actual cause and even in the consideration of vaccines; really??? How much evidence would be enough. And ASD does NOT involve only the aluminum adjuvants, but as well the MMR vaccine, one or both and all vaccines being clearly and potentially causative. Look at the varied means that have been used to recover these children. That clearly suggests vaccines in general. The epidemiological studies that have been conducted have never looked at anything but the MMR vaccine, and Thimerosal. None of those studies looked at anything else in regard to vaccines. As well there has never been any epidemiological studies done comparing vaccinated verses entirely unvaccinated, health outcomes. Do you think it is long past time that were done? I do.

They at the CDC, do KNOW; and they have known all along! Are we really supposed to believe that all of vaccine safety, is adequately addressed using only CDC funded epidemiological studies done on only one vaccine, (MMR); and one single vaccine ingredient, (Thimerosal). That is all that is necessary to prove vaccine safety, and the doctors and the mislead and willing sheeple, all believed it, and continue to believe it. Really? The whole vaccine program needs to be shut down on so many multiple levels of evidence of vaccine harm and potential harm, it is literally mind boggling. This 100 year vaccine safety and effectiveness lie, has lasted, long enough.

Lupus. 2012 Feb;21(2):203-9. doi: 10.1177/0961203311429553. Induction of the 'ASIA' syndrome in NZB/NZWF1 mice after injection of complete Freund's adjuvant (CFA).Division of Rheumatology, Department of Clinical and Experimental Medicine, University of Padova, Italy. Abstract Adjuvants, commonly used in vaccines, may be responsible for inducing autoimmunity and autoimmune diseases, both in humans and mice. The so-called 'ASIA' (Autoimmune/inflammatory Syndrome Induced by Adjuvants) syndrome has been recently described, which is caused by the exposure to a component reproducing the effect of adjuvants. The aim of our study was to evaluate the effect of injection of complete Freund's adjuvant (CFA) in NZB/NZWF1 mice, a lupus-prone murine model. We injected 10 NZB/NZWF1 mice with CFA/PBS and 10 with PBS, three times, 3 weeks apart, and followed-up until natural death. CFA-injected mice developed both anti-double-stranded DNA and proteinuria earlier and at higher levels than the control group. Proteinuria-free survival rate and survival rate were significantly lower in CFA-treated mice than in the control mice (p = 0.002 and p = 0.001, respectively). Histological analyses showed a more severe glomerulonephritis in CFA-injected mice compared with the control mice. In addition, lymphoid hyperplasia in spleen and lungs, myocarditis, and vasculitis were observed in the former, but not in the latter group. In conclusion, the injection of CFA in NZB/NZWF1 mice accelerated autoimmune manifestations resembling 'ASIA' syndrome in humans.http://www.ncbi.nlm.nih.gov/pubmed/22235054 Lupus. 2012 Feb;21(2):146-52. doi: 10.1177/0961203311429318. Autoimmunity following hepatitis B vaccine as part of the spectrum of 'Autoimmune (Auto-inflammatory) Syndrome induced by Adjuvants' (ASIA): analysis of 93 cases. Source: The Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel. CONCLUSIONS: Common clinical characteristics were observed among 93 patients diagnosed with immune-mediated conditions post-HBVv, suggesting a common denominator in these diseases. In addition, risk factors such as history of autoimmune diseases and the appearance of adverse event(s) during immunization may serve to predict the risk of post-immunization diseases. The ASIA criteria were found to be very useful among adults with post-vaccination events. The application of the ASIA criteria to pediatric populations requires further study.http://www.ncbi.nlm.nih.gov/pubmed/22235045Lupus. 2009 Nov;18(13):1192-7. doi: 10.1177/0961203309345732.Ten cases of systemic lupus erythematosus related to hepatitis B vaccine.enter for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel. Data from this case-series, and previously documented cases in the literature could only show a temporal relation between hepatitis B vaccination and the appearance of systemic lupus erythematosus. Systemic lupus erythematosus related to vaccine may differ from idiopathic systemic lupus erythematosus in its clinical presentation and may resemble drug-induced systemic lupus erythematosus. Thus, physicians should be alerted to this potential association, its possible long latency period and unique presentations, and be encouraged to report and analyze these cases.http://www.ncbi.nlm.nih.gov/pubmed/19880567 Systemic lupus erythematosus following HPV immunization or infection? SUMMARY: These cases narrate instances of the onset or exacerbation of lupus following HPV immunization suggesting adjuvant-induced autoimmunity. On the other hand, there are reports of higher incidence of HPV infection in SLE, with the infection per se possibly contributing to disease activity. Thus, the benefit of HPV immunization may still outweigh the risk among these individualshttp://www.ncbi.nlm.nih.gov/pubmed/22235047 And they yet above, find another inept way to justify still justify the vaccine. In healthy persons HPV normally resolves itself in time with no adverse effect; by the immune system itself. Only compromised persons would have an issue, and of course those previously healthy and now compromised by the toxicity of the vaccine Nat Rev Rheumatol. 2009 Nov;5(11):648-52. doi: 10.1038/nrrheum.2009.196. Vaccines and autoimmunity. Center for Autoimmune Diseases and Department of Medicine B, Sheba Medical Center, Sheba Medical Center, Tel-Hashomer, Israel. In this article, on the basis of published evidence and our own experience, we discuss the various aspects of the causal and temporal interactions between vaccines and autoimmune phenomena, as well as the possible mechanisms by which different components of vaccines might induce autoimmunityhttp://www.ncbi.nlm.nih.gov/pubmed/19865091 IFNα causes systemic lupus erythematosus and possibly mediates self-organized criticality theory of autoimmunity Objectives: The pathogenesis of SLE is unclear. Overstimulation of CD4 T cells by antigen led to the development of autoantibody-inducing CD4 T (aiCD4 T) cell capable of inducing autoantibodies and lupus tissue disease. In this novel ‘Self-organized criticality theory of autoimmunity’, we noted that aiCD4 T cell is induced via de novo TCR revision. We now test IFNα as a mediator for the induction of aiCD4 T cell to cause SLE. Conclusions: IFNα is responsible for the core manifestation of SLE, and may induce lupus tissue injury via DN T cells.http://jimmunol.org/cgi/content/meeting_abstract/186/1_MeetingAbstracts/44.47 Immunol Today. 1989 Jul;10(7):246-51.The role of interleukin 2 in autoimmunity.http://www.ncbi.nlm.nih.gov/pubmed/2679638 Research Article Interleukin 2 production in a family with systemic lupus erythematosus and a C4Q0 heterozygous inheritance. Abstract Interleukin 2 production was studied in a family with systemic lupus erythematosus (SLE) and a C4Q0 heterozygous inheritance. Autoimmune manifestations seemed to be associated with the HLA haplotype containing the C4Q0 allele, which was shared by all four ill family members. Concentrations of interleukin 2, however, did not associate either with the haplotype or with the clinical or serological manifestations, as diminished concentrations of interleukin 2 were found in only two subjects with SLE. Thus the defect in this family seemed to be acquired rather than genetically conditioned.http://ard.bmj.com/content/50/8/579.short Self-organized criticality-(definition) From Wikipedia, the free encyclopedia In physics, self-organized criticality (SOC) is a property of (classes of) dynamical systems which have a critical point as an attractor. Their macroscopic behaviour thus displays the spatial and/or temporal scale-invariance characteristic of the critical point of a phase transition, but without the need to tune control parameters to precise values.http://en.wikipedia.org/wiki/Self-organized_criticality COMPLETE proof below, that they do NOT have a clue what these vaccines are doing! The complete knowledge is obviously NOT there. No where even near to enough. Arthur Weiss, MD, PhDTitle ProfessorHoward Hughes Investigator School UCSF School of MedicineDepartment of Medicine Overview Research Interest: The response of lymphocytes to antigen which initiates an antigen specific immune response also represents a unique opportunity to study how complex molecular interactions between cells can lead to developmental decisions, cell differentiation and proliferation. We are interested in understanding how receptors involved in antigen recognition can initiate signal transduction events that regulate cell responses in the immune system. We know that receptors involved in antigen recognition functionally interact with tyrosine kinases and phosphatases, enzymes that regulate protein phosphorylation, to induce signaling pathways that regulate cellular responses and gene expression. We are using genetically selective small molecule inhibitors of kinases together with phosphatase mutants to study how thresholds for the initiation of immune responses are set and how feedback circuits influence responses. We would like to understand how the tyrosine kinases and phosphatases in these pathways are regulated and how they control cellular responses in development, in normal immune responses and in autoimmune diseases such as lupus and rheumatoid arthritis.http://profiles.ucsf.edu/arthur.weissAluminum information, toxicity, safety, danger, benefit and risk From: History of crime against the Food Laws (1929) by Dr. Riley, the prime mover behind the original Pure Food Law and Director of the FDA. He resigned in disgust in 1912 over exceptions granted to the law and lack of enforcement. Aluminum has been exempted from testing for safety by the FDA under a convoluted logic wherein it is classified as GRAS. (Generally Regarded As Safe.) It has never been tested by the FDA on its safety and there are NO restrictions whatever on the amount or use of aluminum. Diseases Associated with Aluminium Intoxication. H. Tomlinson, M.B., Ch.B., MRCS., LRCP. Since that time thousands of studies have been published indicating aluminum is involved in neurological dysfunction, immunocompetence, as well as a host of other morbidities. I cannot begin to reference them all. Sepsis: a cause of aluminum release from tissue stores associated with acute neurological dysfunction and mortality. Davenport A. – Williams P.S. – Roberts N.B. – Bone J.M. From: Clin Nephrol (1988 Jul) 30(1):48-51. We report six cases of patients with renal failure and exposure to aluminum who developed septicemia. In all cases the serum aluminum increased markedly. This may have contributed to the neurological dysfunction seen in five, and the deaths of four of the patients. We suggest that the rise in serum aluminum was due to the release of tissue-bound aluminum, resulting in an increase in free, diffusable aluminum and that this jeopardized both neurological function and immunocompetence. Understanding Colloidal Suspensions - Help from Frank Hartman & Thomas Riddickhttp://www.raysahelian.com/aluminum.html --------------- Understanding Colloidal Suspensions - Help from Frank Hartman & Thomas Riddick Aluminum toxicity is a widespread problem in all forms of life, including humans, animals, fish, plants and trees, and causes widespread degradation of the environment and health. Over 7000 reference articles on aluminum toxicity exist in various data bases; ( as of 1996 ) all recognizing the toxicity but concluding the mechanism of action is unknown. — [ Search results - scirus.com ]Check out the massive number of references on aluminum in general.http://www.scirus.com/srsapp/search?q=%22aluminum+toxicity%22&ds=web#resultsAlum adjuvant boosts adaptive immunity by inducing uric acid and activating inflammatory dendritic cells. Alum (aluminum hydroxide) is the most widely used adjuvant in human vaccines, but the mechanism of its adjuvanticity remains unknown. In vitro studies showed no stimulatory effects on dendritic cells (DCs). In the absence of adjuvant, Ag was taken up by lymph node (LN)–resident DCs that acquired soluble Ag via afferent lymphatics, whereas after injection of alum, Ag was taken up, processed, and presented by inflammatory monocytes that migrated from the peritoneum, thus becoming inflammatory DCs that induced a persistent Th2 response. The enhancing effects of alum on both cellular and humoral immunity were completely abolished when CD11c+ monocytes and DCs were conditionally depleted during immunization. Mechanistically, DC-driven responses were abolished in MyD88-deficient mice and after uricase treatment, implying the induction of uric acid. These findings suggest that alum adjuvant is immunogenic by exploiting “nature's adjuvant,” the inflammatory DC through induction of the endogenous danger signal uric acid. [These findings suggest that alum adjuvant is immunogenic by exploiting “nature's adjuvant,” the inflammatory DC through induction of the endogenous danger signal uric acid.] Does THAT sound like it would be healthy, and/or that it would promote good health, and strong properly functioning immune system? (Of course not).http://jem.rupress.org/content/205/4/869 DNA released from dying host cells mediates aluminum adjuvant activity Excerpts: Furthermore, we propose that host DNA signaling differentially regulates IgE and IgG1 production after alum-adjuvanted immunization. We suggest that, on the one hand, host DNA induces primary B cell responses, including IgG1 production, through interferon response factor 3 (Irf3)-independent mechanisms. On the other hand, we suggest that host DNA also stimulates 'canonical' T helper type 2 (TH2) responses, associated with IgE isotype switching and peripheral effector responses, through Irf3-dependent mechanisms. The finding that host DNA released from dying cells acts as a damage-associated molecular pattern that mediates alum adjuvant activity may increase our understanding of the mechanisms of action of current vaccines and help in the design of new adjuvants. [And they deny that vaccines dysregulate the immune system and cause allergy? They do not have a clue, nor care to want to.] Aluminum-based adjuvants (aluminum salts or alum) are widely used in human vaccination, although their mechanisms of action are poorly understood. Here we report that, in mice, alum causes cell death and the subsequent release of host cell DNA, which acts as a potent endogenous immunostimulatory signal mediating alum adjuvant activity. Furthermore, we propose that host DNA signaling differentially regulates IgE and IgG1 production after alum-adjuvanted immunization. We suggest that, on the one hand, host DNA induces primary B cell responses, including IgG1 production, through interferon response factor 3 (Irf3)-independent mechanisms. On the other hand, we suggest that host DNA also stimulates ‘canonical’ T helper type 2 (TH2) responses, associated with IgE isotype switching and peripheral effector responses, through Irf3-dependent mechanisms. The finding that host DNA released from dying cells acts as a damage-associated molecular pattern that mediates alum adjuvant activity may increase our understanding of the mechanisms of action of current vaccines and help in the design of new adjuvants.http://www.nature.com/nm/journal/v17/n8/full/nm.2403.htmlhttp://www.ncbi.nlm.nih.gov/pubmed/21765404 Perfect alteration of the immune system to produce increased allergies, and what is on the major increase; childhood allergies? Potential allergy induced to as well to any substance in the vaccine, and as well as self cells; autoimmune diseases. (See the plosONE study as well). Cutting Edge: Alum Adjuvant Stimulates Inflammatory Dendritic Cells through Activation of the NALP3 Inflammasome Excerpt: We propose that, in addition to TLR stimulators, agonists of the NALP3 inflammasome should also be considered as vaccine adjuvants. [So obviously they think that chronic inflammation in the body and brain is a necessary, good, and healthy thing, to stay healthy and free of disease? Mindless!!!!http://www.jimmunol.org/content/181/6/3755.short 3-10 The Toll-Like Receptor Family of Innate Immune Receptors Recognition of conserved microbial components by Toll-like receptors leads to inflammation and activation of sentinel immune cells Stimulation of macrophages or mast cells through their Toll-like receptors leads to the synthesis and secretion of proinflammatory cytokines and lipid mediators, thereby initiating the inflammatory response that recruits both soluble immune components and immune cells from the blood, and which we describe in later sections. TLR stimulation of dendritic cells induces the initiation of an adaptive immune response, as we shall see in the next chapter. In this section and the next we shall focus on the structural and functional features of this family of receptors that enable it to detect the presence of infection and tosignal an appropriate response.http://www.sinauer.com/pdf/nsp-immunity-3-10.pdf SO MUCH FOR ANY DENIAL THAT VACCINES ARE THE CAUSE OF THE SAID FOUND BRAIN INFLAMMATION, that they know as well want to cluelessly and ignorantly call, "Dysregulation Syndromes", and as if there is something wrong with the child, or genetically. Actually realize how many times here that this said chronic brain inflammation has now been found in those with ASD? And you know, that as a fact a lot of these children have that inflammation, and likely never acquired ASD. ADHD, ADD, learning disorders, behavioral problems, etc. That's right, now you get the picture. Safe and effective, we looked at all the studies? CDC funded predetermined outcome, and flawed study design epidemiological studies, on one vaccine and one single ingredient, covered it all? Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegenerationhttp://www.ncbi.nlm.nih.gov/pubmed/17119290 “Brain zinc uptake is facilitated by L- and D-histidine, but a transporter, if involved, has not been identified”. Silencing of ZnT1 reduces Zn2+ efflux in cultured cortical neuronshttp://crab-lab.zool.ohiou.edu/colvin/letters09.pdf--------------- Chapter V: 2003 It's Rotten in Denmark, (the Denmark study)http://www.putchildrenfirst.org/chapter5.htmlWhen you look at studies, you also need to consider as well other information that puts the whole picture into its proper focus. No information should be left off limits. International Review of Psychiatry, December 2005; 17(6): 485–495 Immunity, neuroglia and neuroinflammation in autismhttp://healing-arts.org/children/mercury_in_vaccines_autism_research/Immunity_Neuroinflammation_Autism_Study.pdf Autism and Fibromyalgia: Can they be Linked as an “Auto-Immune” Disorder Originating In-Utero? Read more:http://guardianlv.com/2012/08/autism-and-fibromyalgia-can-they-be-linked-as-an-auto-immune-disorder-originating-in-utero/ So, now they are calling all these things and incorrectly, Dysregulation Spectrum Syndromes. They clearly seem to be claiming the cause is unknown; and then they also claim (without reference, I might add); that it is believed that the condition is developed in-utero as an inflammatory syndrome of sorts, similar to fibromyalgia and many other syndromes. WHERE is their evidence of that, in significant numbers of people? It is a guess??? Well, it sure looks like that is what it is, only a guess. How do they actually disregard the fact that entirely bright and healthy children exist, and then when give such as the MMR and/or a load of other vaccines, that all of a sudden the child is very ill, and then starts the progression to all of the symptoms that end up even lost speech, totally disconnected from functional reality, flapping arms, out of control AUTISM??? They want to entirely overlook that in their scenario of situation. Dysregulation Spectrum Syndromeshttp://www.overcomefibro.com/fibro-symptoms-dysregulation-syndrome.html And what do we have right here, in the next below study? You guessed it. Fibromyalgia, infection and vaccination: Two more parts in the etiological puzzle Jacob N. Ablina, , , Yehuda Shoenfeldb, Dan Buskilac a Department of Rheumatology, Tel-Aviv Sourasky Medical Center and Sackler Faculty of Medicine, Tel-Aviv University, 6 Weizman St., 64239 Tel-Aviv, Israel Abstract As the pathogenesis of fibromyalgia continues to raise debate, multiple putative triggers have been implicated. The current review summarizes the available data linking fibromyalgia to either infection or vaccination. Multiple infectious agents have been associated with the development of either full-blown fibromyalgia (e.g. hepatits C), or with symptom complexes extensively overlapping with that syndrome (e.g. chronic Lyme disease). The cases of Lyme disease, mycoplasma, hepatits C and HIV are detailed. Despite the described associations, no evidence is available demonstrating the utility of antibiotic or anti-viral treatment in the management of fibromyalgia. Possible mechanistic links between fibromyalgia and HIV are reviewed. Associations have been described between various vaccinations and symptom complexes including fibromyalgia and chronic fatigue syndrome. The case of Gulf War syndrome, a functional multisystem entity sharing many clinical characteristics with fibromyalgia is discussed, with emphasis on the possibility of association with administration of multiple vaccinations during deployment in the Persian Gulf and the interaction with stress and trauma. Based on this example a model is proposed, wherein vaccinations function as co-triggers for the development of functional disorders including fibromyalgia, in conjunction with additional contributing factors.http://www.sciencedirect.com/science/article/pii/S0896841106000795 There you have it! Plain and simple. [Based on this example a model is proposed, wherein vaccinations function as co-triggers for the development of functional disorders including fibromyalgia, in conjunction with additional contributing factors.] Think, their wrong??? An Immune Disorder at the Root of Autism Excerpts: So here’s the short of it: At least a subset of autism — perhaps one-third, and very likely more — looks like a type of inflammatory disease. And it begins in the womb. It starts with what scientists call immune dysregulation. Ideally, your immune system should operate like an enlightened action hero, meting out inflammation precisely, accurately and with deadly force when necessary, but then quickly returning to a Zen-like calm. Doing so requires an optimal balance of pro- and anti-inflammatory muscle. In autistic individuals, the immune system fails at this balancing act. Inflammatory signals dominate. Anti-inflammatory ones are inadequate. A state of chronic activation prevails. And the more skewed toward inflammation, the more acute the autistic symptoms. Nowhere are the consequences of this dysregulation more evident than in the autistic brain. Spidery cells that help maintain neurons — called astroglia and microglia — are enlarged from chronic activation. Pro-inflammatory signaling molecules abound. Genes involved in inflammation are switched on. These findings are important for many reasons, but perhaps the most noteworthy is that they provide evidence of an abnormal, continuing biological process. That means that there is finally a therapeutic target for a disorder defined by behavioral criteria like social impairments, difficulty communicating and repetitive behaviors. Read more:http://www.nytimes.com/2012/08/26/opinion/sunday/immune-disorders-and-autism.html?_r=1&pagewanted=all Introductions to the scientific work related to autism of V. K. Singh, Ph.D.http://www.vaccinationnews.com/DailyNews/June2002/FindingsImmunology30.htm Aluminum and Vaccines — A Brain-Destroying Duo, Says Top Doc Common vaccines that contain aluminum include: • DTaP (diphtheria, tetanus, and pertussis) — 625 mcg • Hepatitis B — 375 mcg • Hepatitis A — 250 mcg • Hib (haemophilus influenza type B) — 225 mcg • PVC (pneumococcoal conjugate vaccine) — 125 mcg • HPV— Gardasil contains 225 mcg in each of the three required doses. Excerpt: Aluminum has been added to vaccines for about 90 years in the belief it spurs the body to produce disease-fighting antibodies. But aluminum is toxic, and many common vaccines, including pneumonia, tetanus, and HPV, contain large doses. The result is children are getting amounts that are much higher than those considered safe by regulatory agencies, and adults are adding to the lifetime cumulative amounts of aluminum in their bodies. These megadoses can have a devastating effect on the brain, says Newsmax Health expert Dr. Russell Blaylock, causing everything from brain damage in children to Alzheimer’s in adults. “Aluminum is toxic,” Dr. Blaylock tells Newsmax Health. “Compelling research has demonstrated that aluminum is an accumulative neurotoxin, even in small concentrations. It has a tendency to concentrate in the hippocampus, an area of the brain vital to crucial functions including learning, memory, and behavior. “Recent articles on aluminum have shown that aluminum in vaccines is producing severe problems in the brains of developing children,” he says. “The evidence is overwhelming, but many officials and doctors ignore it. They refuse to look at the evidence because it scares them — it’s powerful evidence. “Of the 36 vaccines children get, 18 of them contain aluminum,” says Dr. Blaylock. “One article showed that children get doses 46 times higher than those considered safe by government agencies.” Read more: http://www.newsmaxhealth.com/headline_health/Aluminum_Vaccines_Brain/2012/02/16/434204.html Safety of Aluminum Added to Vaccines as a Vaccine Adjuvant, (more aluminum adjuvant harm studies) http://www.iaomt.org/testfoundation/aluminumvaccines.htm Adverse Effects of Vaccines: Evidence and Causality (2012)http://www.nap.edu/openbook.php?record_id=13164&page=R9 100 Compiled Studies on Vaccine Dangershttp://www.activistpost.com/2011/09/100-compiled-studies-on-vaccine-dangers.html Vaccines and Scientific Studieshttp://www.thinktwice.com/studies.htm Autism/vaccine studies: multiple morehttp://www.tacanow.org/wp-content/uploads/2011/09/autism-studies-april-2008.pdf Brain Behav Immun. 1993 Mar;7(1):97-103. Antibodies to myelin basic protein in children with autistic behavior Singh VK, Warren RP, Odell JD, Warren WL, Cole P. Source;Biomedical Division, Center for Persons with Disabilities, Logan, Utah.http://www.ncbi.nlm.nih.gov/pubmed/7682457 Taming brain inflammation A common factor in many brain disorders, including brain fog, ADHD, ADD, anxiety, depression, memory loss, is brain inflammation.http://brain-dr.com/taming-brain-inflammation/ “Following Vaccinations” — 900 Voices Telling the Truth http://www.ageofautism.com/2011/06/following-vaccinations-900-voices-telling-the-truth.html Parents Voice: Children’s Adverse Outcomes Following Vaccination http://www.followingvaccinations.com/ How much aluminum is in the vaccines. You may be entirely shocked by how much. No safety studies have EVER been done. Aluminum was given an FDA status of (GRAS) generally regarded as safe, in 1929 and even though aluminum has been used as a vaccine adjuvant for decades, NO safety studies have been done. Amount of aluminum in vaccines – detailed list “ActHib – 0 mcg PedVaxHib – 225 mcg Prevnar – 125 mcg Daptacel (DTaP) – 330 mcg Tripedia (DTaP) – 170 mcg Infanrix (DTaP) – 625 mcg Recombivax (HepB) – 250 mcg Engerix B (HepB) – 250 mcg Polio – 0 mcg MMR – 0 mcg Chic Pox – 0 mcg Hep A – 250 mcg Combo Vaccines: Comvax (hep B as Recombivax and HIB as PedVaxHIB) – 225 mcg. This particular combo vax has LESS aluminum than getting the shots separately. Pentacel (DTaP as Daptacel, HIB as ActHIB and polio) – 1500 mcg. This shot has a lot MORE aluminum that the sum of its parts. You actually get 5 times the amount of aluminum than if you were to get the shots separately. Pediarix (DTaP as Infanrix, hepB as EngerixB and polio) – 850 mcg TriHIBit (DTaP as Tripedia and HIB as ActHIB) – 170 mcg”http://www.mothering.com/community/t/815768/amount-of-aluminum-in-vaccines-detailed-list Vaccine Ingredients — A Comprehensive Guidehttp://vaxtruth.org/2011/08/vaccine-ingredients/Review Fibromyalgia, infection and vaccination: Two more parts in the etiological puzzlehttp://www.sciencedirect.com/science/article/pii/S0896841106000795 Mercury and Aluminum in Vaccines: a Primer on NVIC’s Vaccine Ingredients Calculator http://vaxtruth.org/2012/01/aluminum-toxicity-and-a-primer-on-the-vic/ Lack Of Aluminum Adjuvant Safety Data SOME EFFECTS OF REDUCED CARRYING CAPACITY Excerpts: Aluminum toxicity is a widespread problem in all forms of life, including humans, animals, fish, plants and trees, and causes widespread degradation of the environment and health. Over 7000 reference articles on aluminum toxicity exist in various data bases; ( as of 1996 ) all recognizing the toxicity but concluding the mechanism of action is unknown. — [ Search results - scirus.com ]http://www.scirus.com/srsapp/search?q=%22aluminum+toxicity%22&ds=mem=jnl&ds=web#results Aluminium in vaccines can cause serious polio-like damage, damage motorneuron cells and cause brain damage – possibly leading to Alzheimer’s and other forms of dementia and increasing the risk in children of Autistic Spectrum Disorders. From the Transcripts of the US Vaccines and Related Biological Advisory Committee Meeting (VRBAC) and Scientific Papers The Experts admitted Ignorancehttp://albamora.com/joanmorahomeopatia/pdf/Aluminum%20in%20Vaccines%20-from%20forthcoming%20book.pdf ASD and Aluminum Toxicity http://drtenpenny.com/Documents/Aluminum%20part%202%20(157%20slide).pdf ————————–

Toxicol Appl Pharmacol. 2006 Jul 15;214(2):99-108. Epub 2006 Jun 16. Porphyrinuria in childhood autistic disorder: implications for environmental toxicity. Nataf R, Skorupka C, Amet L, Lam A, Springbett A, Lathe R. SourceLaboratoire Philippe Auguste, Paris, France. Toxicol Appl Pharmacol. 2006 Jul 15;214(2):99-108. Epub 2006 Jun 16. Porphyrinuria in childhood autistic disorder: implications for environmental toxicity. Nataf R, Skorupka C, Amet L, Lam A, Springbett A, Lathe R. SourceLaboratoire Philippe Auguste, Paris, France.http://www.ncbi.nlm.nih.gov/pubmed?term=PMID%3A%2016782144 Again, if the medical side is ALL about the science; then why do they refuse to look at nor acknowledge the bulwark of vaccine harm science that exists? Just because the CDC refuses to acknowledge those studies, does it make them invalid? And as said, did you know that in 1929 as well that the FDA gave the substance aluminum, a rated status of (GRAS), generally regarded as safe? Even after put in vaccines in the form of an adjuvant, no safety studies have been done, nor does any sufficient safety data exist. The CDC admits to that right in their own documents. In their documents they clearly put out an assessment of need and the request for additional studies and data. It simply has not been happening. They already know what the result would be. ————————– Research Article The Severity of Autism Is Associated with Toxic Metal Body Burden and Red Blood Cell Glutathione Levels Abstract This study investigated the relationship of children’s autism symptoms with their toxic metal body burden and red blood cell (RBC) glutathione levels. In children ages 3–8 years, the severity of autism was assessed using four tools: ADOS, PDD-BI, ATEC, and SAS. Toxic metal body burden was assessed by measuring urinary excretion of toxic metals, both before and after oral dimercaptosuccinic acid (DMSA). Multiple positive correlations were found between the severity of autism and the urinary excretion of toxic metals. Variations in the severity of autism measurements could be explained, in part, by regression analyses of urinary excretion of toxic metals before and after DMSA and the level of RBC glutathione (adjusted in all cases). This study demonstrates a significant positive association between the severity of autism and the relative body burden of toxic metals.http://www.hindawi.com/journals/jt/2009/532640/ Oxidative Stress Causes Renal Dopamine D1 Receptor Dysfunction and Hypertension via Mechanisms That Involve Nuclear Factor-? B and Protein Kinase C http://jasn.asnjournals.org/content/18/5/1446.long Low natural killer cell cytotoxic activity in autism: The role of glutathione, IL-2 and IL-15 http://www.sciencedirect.com/science/article/pii/S0165572808003986 Oxidative stress in autism NYS Institute for Basic Research in Developmental Disabilities Excerpt: Several studies have suggested alterations in the activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and catalase in autism. Additionally, altered glutathione levels and homocysteine/methionine metabolism, increased inflammation, excitotoxicity, as well as mitochondrial and immune dysfunction have been suggested in autismhttp://www.sciencedirect.com/science/article/pii/S0928468006000538 Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism Excerpt: These results suggest that the autism LCLs exhibit a reduced glutathione reserve capacity in both cytosol and mitochondria that may compromise antioxidant defense and detoxification capacity under prooxidant conditions.http://www.fasebj.org/content/23/8/2374.short Neurotoxicology. 2005 Jan;26(1):1-8. Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors. http://www.ncbi.nlm.nih.gov/pubmed/15527868 Induction of Oxidative Stress by Glutathione Depletion Causes Severe Hypertension in Normal Rats http://www.ncbi.nlm.nih.gov/pubmed/10904027http://hyper.ahajournals.org/content/36/1/142.full.pdfhttp://ndt.oxfordjournals.org/content/18/8/1439.full.pdf

This below study, shows that even though ethyl mercury may be detoxed more quickly as far as the amount leaving the body; the study shows that both ethyl mercury and methyl mercury are still a significant concern as to potential toxicity. As well just because ethyl mercury left the body quicker, that would not tell you what level of mercury was left in the tissues, organs, and the brain. Such statements would as well clearly not take in account the children and adults who produce less that adequate levels of glutathione necessary to detox that ethyl mercury. Arch Toxicol. 1985 Sep;57(4):260-7. The comparative toxicology of ethyl- and methylmercury. Magos L, Brown AW, Sparrow S, Bailey E, Snowden RT, Skipp WR. Abstract Neurotoxicity and renotoxicity were compared in rats given by gastric gavage five daily doses of 8.0 mg Hg/kg methyl- or ethylmercuric chloride or 9.6 mg Hg/kg ethylmercuric chloride. Three or 10 days after the last treatment day rats treated with either 8.0 or 9.6 mg Hg/kg ethylmercury had higher total or organic mercury concentrations in blood and lower concentrations in kidneys and brain than methylmercury-treated rats. In each of these tissues the inorganic mercury concentration was higher after ethyl- than after methylmercury. Weight loss relative to the expected body weight and renal damage was higher in ethylmercury-treated rats than in rats given equimolar doses of methylmercury. These effects became more severe when the dose of ethylmercury was increased by 20%. Thus in renotoxicity the renal concentration of inorganic mercury seems to be more important than the concentration of organic or total mercury. In methylmercury-treated rats damage and inorganic mercury deposits were restricted to the P2 region of the proximal tubules, while in ethylmercury-treated rats the distribution of mercury and damage was more widespread. There was little difference in the neurotoxicities of methylmercury and ethylmercury when effects on the dorsal root ganglia or coordination disorders were compared. Based on both criteria, an equimolar dose of ethylmercury was less neurotoxic than methylmercury, but a 20% increase in the dose of ethylmercury was enough to raise the sum of coordination disorder scores slightly and ganglion damage significantly above those in methylmercury-treated rats.http://www.ncbi.nlm.nih.gov/pubmed/4091651 And how can they they at the CDC, keep on recommending the flu shot for all pregnant women that contains 25 mcg. of thimerosal, (mercury)???? Mercury Poisoning Is a Growing Menacehttp://readersupportednews.org/opinion2/271-38/15500-focus-mercury-poisoning-is-a-growing-menace Brain Dev. 2012 May 31. [Epub ahead of print] Prenatal exposure to organomercury, thimerosal, persistently impairs the serotonergic and dopaminergic systems in the rat brain: Implications for association with developmental disorders. Ida-Eto M, Oyabu A, Ohkawara T, Tashiro Y, Narita N, Narita M. Source:Department of Anatomy II, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan. Abstract Thimerosal, an organomercury compound, has been widely used as a preservative. Therefore, concerns have been raised about its neurotoxicity. We recently demonstrated perturbation of early serotonergic development by prenatal exposure to thimerosal (Ida-Eto et al. (2011) [11]). Here, we investigated whether prenatal thimerosal exposure causes persistent impairment after birth. Analysis on postnatal day 50 showed significant increase in hippocampal serotonin following thimerosal administration on embryonic day 9. Furthermore, not only serotonin, striatal dopamine was significantly increased. These results indicate that embryonic exposure to thimerosal produces lasting impairment of brain monoaminergic system, and thus every effort should be made to avoid the use of thimerosal.http://www.ncbi.nlm.nih.gov/pubmed/22658806

Neurosci Lett. 2011 Nov 14;505(2):61-4. doi: 10.1016/j.neulet.2011.05.053. Epub 2011 Jun 6.Embryonic exposure to thimerosal, an organomercury compound, causes abnormal early development of serotonergic neurons.http://www.ncbi.nlm.nih.gov/pubmed/21669256 Brain Dev. 2013 Mar;35(3):261-4. doi: 10.1016/j.braindev.2012.05.004. Epub 2012 Jun 1.Prenatal exposure to organomercury, thimerosal, persistently impairs the serotonergic and dopaminergic systems in the rat brain: Implications for association with developmental disorders.http://www.ncbi.nlm.nih.gov/pubmed/22658806 Maternal transfer of mercury to the developing embryo/fetus: is there a safe level? Mercury (Hg) exposure is ubiquitous in modern society via vaccines, fish/crustacea, dental amalgam, food, water, and the atmosphere. This article examines Hg exposure in the context of primary exposure to pregnant women and secondary exposure experienced by their unborn babies. Babies in utero are particularly at risk of higher Hg exposure than adults (on a dose/weight basis through maternal Hg transfer via the placenta), and are more susceptible to adverse effects from mercury and its biologically active compounds. It is, therefore, critical that regulatory advisories around maximum safe Hg exposures account for pregnant women and secondary exposure that children in utero experience. This study focused on standardized embryonic and fetal Hg exposures via primary exposure to the pregnant mother of two common Hg sources (dietary fish and parenteral vaccines). Data demonstrated that Hg exposures, particularly during the first trimester of pregnancy, at well-established dose/weight ratios produced severe damage to humans including death. In light of research suggestive of a mercuric risk factor for childhood conditions such as tic disorders, cerebral palsy, and autism, it is essential that Hg advisories account for secondary prenatal human exposures. Source: Toxicological and Environmental Chemistry, http://www.tandfonline.com/doi/abs/10.1080/02772248.2012.724574 Prenatal Exposure to Mercury and Fish Consumption During Pregnancy and Attention-Deficit/Hyperactivity Disorder–Related Behavior in Childrenhttp://archpedi.jamanetwork.com/article.aspx?articleid=1377487 DNA released from dying host cells mediates aluminum adjuvant activity Abstract Aluminum-based adjuvants (aluminum salts or alum) are widely used in human vaccination, although their mechanisms of action are poorly understood. Here we report that, in mice, alum causes cell death and the subsequent release of host cell DNA, which acts as a potent endogenous immunostimulatory signal mediating alum adjuvant activity. Furthermore, we propose that host DNA signaling differentially regulates IgE and IgG1 production after alum-adjuvanted immunization. We suggest that, on the one hand, host DNA induces primary B cell responses, including IgG1 production, through interferon response factor 3 (Irf3)-independent mechanisms. On the other hand, we suggest that host DNA also stimulates 'canonical' T helper type 2 (TH2) responses, associated with IgE isotype switching and peripheral effector responses, through Irf3-dependent mechanisms. The finding that host DNA released from dying cells acts as a damage-associated molecular pattern that mediates alum adjuvant activity may increase our understanding of the mechanisms of action of current vaccines and help in the design of new adjuvants.http://www.nature.com/nm/journal/v17/n8/full/nm.2403.html And instead of in the above study, making any condemnation of aluminum adjuvants in current vaccines, they only propose the design of new adjuvants; which so far have proven to have caused and be causing even more problems and potential harm. New Generation of Vaccine Adjuvants: Worst Ever?http://gaia-health.com/gaia-blog/2013-01-26/new-generation-of-vaccine-adjuvants-worst-ever/

Toxicological Status of Children with Autism vs. Neurotypical Children and the Association with Autism Severity James B. Adams, Tapan Audhya, Sharon McDonough-Means, Robert A. Rubin, David Quig, Elizabeth Geis, Eva Gehn, Melissa Loresto, Jessica Mitchell, Sharon Atwood, … show all 12 Abstract This study investigates both the level of toxic metals in children with autism and the possible association of those toxic metals with autism severity. This study involved 55 children with autism ages 5–16 years compared to 44 controls with similar age and gender. The study included measurements of toxic metals in whole blood, red blood cells (RBC), and urine. The autism group had higher levels of lead in RBC (+41 %, p = 0.002) and higher urinary levels of lead (+74 %, p = 0.02), thallium (+77 %, p = 0.0001), tin (+115 %, p = 0.01), and tungsten (+44 %, p = 0.00005). However, the autism group had slightly lower levels of cadmium in whole blood (−19 %, p = 0.003). A stepwise, multiple linear regression analysis found a strong association of levels of toxic metals with variation in the degree of severity of autism for all the severity scales (adjusted R 2 of 0.38–0.47, p < 0.0003). Cadmium (whole blood) and mercury (whole blood and RBC) were the most consistently significant variables. Overall, children with autism have higher average levels of several toxic metals, and levels of several toxic metals are strongly associated with variations in the severity of autism for all three of the autism severity scales investigated.http://link.springer.com/article/10.1007%2Fs12011-012-9551-1 This, is not exactly a strong case for the continued use of flu shots with Thimerosal, in pregnant women. Nothing would be enough. None of these studies are!Mitochondrial Dysfunction Wow, great information article, but not a mention of vaccines, even though Pubmed and multiple studies on the effect, and as well in regard to glutathione. And also not a mention of the success of biomedical treatment.http://www.epidemicanswers.org/mitochondrial-dysfunction/ Lasting neuropathological changes in rat brain after intermittent neonatal administration of thimerosal. Olczak M, Duszczyk M, Mierzejewski P, Wierzba-Bobrowicz T, Majewska MD. Source Department of Pharmacology and Physiology of the Nervous System, Institute of Psychiatry and Neurology, ul. Sobieskiego 9, Warsaw, Poland. Abstract Thimerosal, an organomercurial added as a preservative to some vaccines, is a suspected iatrogenic factor, possibly contributing to paediatric neurodevelopmental disorders including autism. We examined the effects of early postnatal administration of thimerosal (four i.m. injections, 12 or 240 µg THIM-Hg/kg, on postnatal days 7, 9, 11 and 15) on brain pathology in Wistar rats. Numerous neuropathological changes were observed in young adult rats which were treated postnatally with thimerosal. They included: ischaemic degeneration of neurons and "dark" neurons in the prefrontal and temporal cortex, the hippocampus and the cerebellum, pathological changes of the blood vessels in the temporal cortex, diminished synaptophysin reaction in the hippocampus, atrophy of astroglia in the hippocampus and cerebellum, and positive caspase-3 reaction in Bergmann astroglia. These findings document neurotoxic effects of thimerosal, at doses equivalent to those used in infant vaccines or higher, in developing rat brain, suggesting likely involvement of this mercurial in neurodevelopmental disorders.http://www.ncbi.nlm.nih.gov/pubmed/21225508 Vaccines and especially aluminum adjuvants cause over activation of the brains microlgia and resulting chronic brain inflammation, and has now been found in both those with ASD and ADHD, in several studies., (Those studies are found as well on this site). Neurotoxicology. 2012 Mar;33(2):191-206. doi: 10.1016/j.neuro.2012.01.012. Epub 2012 Feb 2. Microglia in the developing brain: a potential target with lifetime effects. Harry GJ, Kraft AD. Source:National Toxicology Program Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Abstract Microglia are a heterogenous group of monocyte-derived cells serving multiple roles within the brain, many of which are associated with immune and macrophage like properties. These cells are known to serve a critical role during brain injury and to maintain homeostasis; yet, their defined roles during development have yet to be elucidated. Microglial actions appear to influence events associated with neuronal proliferation and differentiation during development, as well as, contribute to processes associated with the removal of dying neurons or cellular debris and management of synaptic connections. These long-lived cells display changes during injury and with aging that are critical to the maintenance of the neuronal environment over the lifespan of the organism. These processes may be altered by changes in the colonization of the brain or by inflammatory events during development. This review addresses the role of microglia during brain development, both structurally and functionally, as well as the inherent vulnerability of the developing nervous system. A framework is presented considering microglia as a critical nervous system-specific cell that can influence multiple aspects of brain development (e.g., vascularization, synaptogenesis, and myelination) and have a long term impact on the functional vulnerability of the nervous system to a subsequent insult, whether environmental, physical, age-related, or disease-related. Published by Elsevier B.V.http://www.ncbi.nlm.nih.gov/pubmed/22322212 Evidence of Parallels Between Mercury Intoxication and the Brain Pathology in Autismhttp://www.bjorklundnutrition.net/2012/08/mercury-and-the-brain-pathology-in-autism/?fb_action_ids=3669587778013&fb_action_types=og.likes&fb_source=aggregation&fb_aggregation_id=246965925417366 New Japanese study confirms mercury in relation to damage in brain structures associated with autismhttp://www.godlikeproductions.com/forum1/message2004889/pg1 Prenatal mercury exposure elevated risk for ADHD-related behavior Sagiv SK. Arch Pediatr Adolesc Med. 2012;doi:10.1001/archpediatrics.2012.1286. November 1, 2012 Excerpt: “These results suggest that prenatal mercury exposure is associated with a higher risk of ADHD-related behaviors, and fish consumption during pregnancy is associated with a lower risk of these behaviors,” Sagiv and colleagues wrote. “Although a single estimate combining these beneficial vs. detrimental effects vis-à-vis fish intake is not possible with these data, these findings are consistent with a growing literature showing risk of mercury exposure and benefits of maternal consumption of fish on fetal brain development and are important for informing dietary recommendations for pregnant women.”http://www.healio.com/pediatrics/add-adhd/news/online/%7B7EEB721F-166C-4DB8-B872-523CCB05ED2D%7D/Prenatal-mercury-exposure-elevated-risk-for-ADHD-related-behavior J Toxicol. 2012; 2012: 373678. Published online 2012 June 28. doi: 10.1155/2012/373678 PMCID: PMC3395253 Thimerosal-Derived Ethylmercury Is a Mitochondrial Toxin in Human Astrocytes: Possible Role of Fenton Chemistry in the Oxidation and Breakage of mtDNA Abstract Thimerosal generates ethylmercury in aqueous solution and is widely used as preservative. We have investigated the toxicology of Thimerosal in normal human astrocytes, paying particular attention to mitochondrial function and the generation of specific oxidants. We find that ethylmercury not only inhibits mitochondrial respiration leading to a drop in the steady state membrane potential, but also concurrent with these phenomena increases the formation of superoxide, hydrogen peroxide, and Fenton/Haber-Weiss generated hydroxyl radical. These oxidants increase the levels of cellular aldehyde/ketones. Additionally, we find a five-fold increase in the levels of oxidant damaged mitochondrial DNA bases and increases in the levels of mtDNA nicks and blunt-ended breaks. Highly damaged mitochondria are characterized by having very low membrane potentials, increased superoxide/hydrogen peroxide production, and extensively damaged mtDNA and proteins. These mitochondria appear to have undergone a permeability transition, an observation supported by the five-fold increase in Caspase-3 activity observed after Thimerosal treatment. 1. Introduction 1.1. Thimerosal and Ethylmercury Thimerosal is a preservative that is widely used in medical products, including as a preservative in vaccines, immunoglobulin preparations, skin test antigens, antivenins, ophthalmic and nasal products, and tattoo inks, and is composed of 49.6 percent ethylmercury by weight [1]. The widespread use of Thimerosal exposes many to its potential toxic effects, especially inutero and in neonates. We report the results of a series of experiments using cultured normal human astrocytes (NHA) exposed to Thimerosal to study the compound's effect on astrocyte mitochondria. 1.2. Oxidative Stress and Brain Read more:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395253/ "Safe, and effective"??? NOVEMBER 11, 2003 Eli Lilly and Thimerosal Excerpts: In the 70 years since thimerosal/Merthiolate was developed, the FDA never required Eli Lilly to conduct clinical studies of its safety, despite ample evidence of its toxicity and its highly allergic properties. In fact, the FDA today still refers to the 1931 Powell and Jameison study on its Web site as indication of the “safety and effectiveness” of thimerosal as a preservative. Thimerosal/Merthiolate was widely used in over-the-counter products, including ointments, eye drops, nasal sprays and contact lens solution. In 1998, the FDA finally banned Thimerosal for use in OTC products—18 years after it began a safety review of mercury-containing products. It took another year before the CDC and the FDA would ask manufacturers to remove thimerosal from childhood vaccines. Eli Lilly stopped making Merthiolate-containing products in the mid-’80s but still profits from licensing agreements with pharmaceutical companies around the world. Eli Lilly may be determined to avoid liability for thimerosal, but that doesn’t mean it has abandoned children with neurological problems. This year, the FDA approved Straterra, a new Eli Lilly drug for the treatment of Attention Deficit Hyperactivity Disorder. The irony that Eli Lilly profits from damaged children is not lost on parent Robert Krakow: “When Eli Lilly is promoting Straterra on TV, saying up to 10 percent of children can be helped, you realize what we are up against.”http://www.inthesetimes.com/article/649/ VRM: Special Report Those doctors who endorse the continued use of Thimerosal in vaccines, including the authors of the recent American Academy of Pediatrics article here-in (Walter A. Orenstein, MD, Jerome A. Paulson, MD, FAAP, Michael T. Brady, MD, FAAP, Louis Z. Cooper, MD, Katherine Seib, MSPH), should have their licences revoked immediately. But it’s also time for conscientious parents to consider walking away, once & for all, from the ENTIRE institution of Western Allopathic Medicine; all the trappings of this Medical Mafia monopoly. You have the evidence in hand. http://vaccineresistancemovement.org/?page_id=11240 Crimes at the CDC (Thimerosal) Excerpts: According to Kennedy, in a July 1999 letter, vaccine producer SmithKline Beecham tells CDC that it is ready to produce non-Thimerosal DTP (Diptheria/Tetanus/Pertussis) vaccines immediately and has sufficient inventories to supply the entire U.S. market during the remainder of 1999 and the first half of 2000, by which time other vaccine manufacturers would have their Thimerosal-free DTP vaccines on line. Thimerosal-laden DTP vaccines containing 25 micrograms of mercury apiece (75 thousand trillion atoms of mercury) were then being administered to American infants at two months, four months and six months — far exceeding EPA’s recommended safe level for mercury. Had CDC accepted SmithKline’s offer, it could have immediately reduced the mercury exposures to vaccinated six-month-old children by 40%. Kennedy continued, “However, in November, CDC mysteriously sent a letter back rejecting SmithKline’s offer. Then, on July 14, 2000 CDC published a deceptive press release promising to require that all vaccines be Thimerosal-free as soon as “adequate supplies are available.” This was a full 12 months after the agency had denied SmithKline’s proposal.” CDC has allowed an entire generation of children to be injured. “If CDC were basing its decision on safety alone, it would have taken SmithKline up on its offer. That’s a no-brainer,” said a federal health official to Kennedy anonymously. “So there were other considerations beside safety that were guiding their decision making.” “Among these “other considerations” were CDC’s important concerns for the preservation of the vaccine program, a bureaucratic impulse for self-preservation, and protecting the economic interests of its vaccine industry friends.”Immediate withdrawal would send a strong message; ‘We messed up!’” the health official told Kennedy. “And I don’t think they wanted to send that message to parents, the public or those considering legal action.” “There was also concern,” says the federal official, “that an immediate withdrawal might discredit the international vaccine programs for which CDC is an important partner.” Why will CDC inject millions of minority kids in America’s poorest neighborhoods with poison proven to kill brain tissue and cause learning disorders when child-safe vaccines are available? - Robert F. Kennedy Jr.http://imva.info/index.php/vaccines/crimes-at-the-cdc/ What's coming through that needle? Dr Sherri Tenpennyhttp://youtu.be/ZlX2O_-ZEu4 What Is Coming Through That Needle? The Problem of Pathogenic Vaccine Contamination Benjamin McReardenhttp://www.scribd.com/doc/42722540/Vaccine-Contamination-Mcrearden Medical evidence shows that pregnant mothers exposed to mercury in vaccines are more likely to have children with ADHDLearn more: http://www.naturalnews.com/038037_pregnancy_vaccines_ADHD.html Multiple studies link autism to mercury, which is still present in most flu vaccinesLearn more: http://www.naturalnews.com/031678_mercury_autism.html Exposed: CDC deliberately manipulated, covered up scientific data showing link between vaccines containing mercury and autism Learn more: http://www.naturalnews.com/034038_vaccines_autism.html Government report links thimerosal laden vaccines to neurological disordersLearn more: http://www.naturalnews.com/036748_thimerosal_vaccines_neurological_disorders.html Vaccines And Immune Suppressionhttp://preventdisease.com/news/articles/vaccines_and_immune_suppresion.shtml Do Vaccines Disable The Immune System?http://www.healthychild.com/do-vaccines-disable-the-immune-system Vaccines and neonatal immune development Hilary Butler - Monday, May 23, 2011http://www.beyondconformity.org.nz/_blog/Hilary's_Desk/post/Vaccines_and_neonatal_immune_development/ Vaccination does not equal immunisationhttp://nocompulsoryvaccination.com/2012/12/24/vaccination-does-not-equal-immunisation/ VIDS – Vaccine Induced Diseaseshttp://www.vaccinesuncensored.org/vids.php A case series of children with apparent mercury toxic encephalopathies manifesting with clinical symptoms of regressive autistic disorders. Abstract J Toxicol Environ Health A. 2007 May 15;70(10):837-51. A case series of children with apparent mercury toxic encephalopathies manifesting with clinical symptoms of regressive autistic disorders. Geier DA, Geier MR. Source:Institute of Chronic Illnesses, Inc., Silver Spring, Maryland, USA. Abstract Impairments in social relatedness and communication, repetitive behaviors, and stereotypic abnormal movement patterns characterize autism spectrum disorders (ASDs). It is clear that while genetic factors are important to the pathogenesis of ASDs, mercury exposure can induce immune, sensory, neurological, motor, and behavioral dysfunctions similar to traits defining or associated with ASDs. The Institutional Review Board of the Institute for Chronic Illnesses (Office for Human Research Protections, U.S. Department of Health and Human Services, IRB number IRB00005375) approved the present study. A case series of nine patients who presented to the Genetic Centers of America for a genetic/developmental evaluation are discussed. Eight of nine patients (one patient was found to have an ASD due to Rett's syndrome) (a) had regressive ASDs; (b) had elevated levels of androgens; (c) excreted significant amounts of mercury post chelation challenge; (d) had biochemical evidence of decreased function in their glutathione pathways; (e) had no known significant mercury exposure except from Thimerosal-containing vaccines/Rho(D)-immune globulin preparations; and (f) had alternate causes for their regressive ASDs ruled out. There was a significant dose-response relationship between the severity of the regressive ASDs observed and the total mercury dose children received from Thimerosal-containing vaccines/Rho (D)-immune globulin preparations. Based upon differential diagnoses, 8 of 9 patients examined were exposed to significant mercury from Thimerosal-containing biologic/vaccine preparations during their fetal/infant developmental periods, and subsequently, between 12 and 24 mo of age, these previously normally developing children suffered mercury toxic encephalopathies that manifested with clinical symptoms consistent with regressive ASDs. Evidence for mercury intoxication should be considered in the differential diagnosis as contributing to some regressive ASDs.http://www.ncbi.nlm.nih.gov/pubmed/17454560 Pubmed index of more related studieshttp://www.ncbi.nlm.nih.gov/pubmed?term=Geier+DA%5BAuthor%5D&cauthor=true&cauthor_uid=17454560 Evidence of Parallels Between Mercury Intoxication and the Brain Pathology in Autismhttp://www.bjorklundnutrition.net/2012/08/mercury-and-the-brain-pathology-in-autism/?fb_action_ids=3669587778013&fb_action_types=og.likes&fb_source=aggregation&fb_aggregation_id=246965925417366 The Severity of Autism Is Associated with Toxic Metal Body Burden and Red Blood Cell Glutathione Levels Abstract This study investigated the relationship of children's autism symptoms with their toxic metal body burden and red blood cell (RBC) glutathione levels. In children ages 3–8 years, the severity of autism was assessed using four tools: ADOS, PDD-BI, ATEC, and SAS. Toxic metal body burden was assessed by measuring urinary excretion of toxic metals, both before and after oral dimercaptosuccinic acid (DMSA). Multiple positive correlations were found between the severity of autism and the urinary excretion of toxic metals. Variations in the severity of autism measurements could be explained, in part, by regression analyses of urinary excretion of toxic metals before and after DMSA and the level of RBC glutathione (adjusted in all cases). This study demonstrates a significant positive association between the severity of autism and the relative body burden of toxic metals.http://www.hindawi.com/journals/jt/2009/532640/ Oxidative Stress Causes Renal Dopamine D1 Receptor Dysfunction and Hypertension via Mechanisms That Involve Nuclear Factor-?B and Protein Kinase Chttp://jasn.asnjournals.org/content/18/5/1446.long Low natural killer cell cytotoxic activity in autism: The role of glutathione, IL-2 and IL-15http://www.sciencedirect.com/science/article/pii/S0165572808003986 Oxidative stress in autism NYS Institute for Basic Research in Developmental Disabilities Excerpt: Several studies have suggested alterations in the activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and catalase in autism. Additionally, altered glutathione levels and homocysteine/methionine metabolism, increased inflammation, excitotoxicity, as well as mitochondrial and immune dysfunction have been suggested in autismhttp://www.sciencedirect.com/science/article/pii/S0928468006000538 Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism Excerpt: These results suggest that the autism LCLs exhibit a reduced glutathione reserve capacity in both cytosol and mitochondria that may compromise antioxidant defense and detoxification capacity under prooxidant conditions.http://www.fasebj.org/content/23/8/2374.short Neurotoxicology. 2005 Jan;26(1):1-8. Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors.http://www.ncbi.nlm.nih.gov/pubmed/15527868 Neurosurgeon issues public challenge to vaccine zealots: Inject yourselves with all shots you say children should get!http://www.naturalnews.com/035335_vaccines_Dr_Blaylock_children.html__________________

The Severity of Autism Is Associated with Toxic Metal Body Burden and Red Blood Cell Glutathione Levels Abstract This study investigated the relationship of children's autism symptoms with their toxic metal body burden and red blood cell (RBC) glutathione levels. In children ages 3–8 years, the severity of autism was assessed using four tools: ADOS, PDD-BI, ATEC, and SAS. Toxic metal body burden was assessed by measuring urinary excretion of toxic metals, both before and after oral dimercaptosuccinic acid (DMSA). Multiple positive correlations were found between the severity of autism and the urinary excretion of toxic metals. Variations in the severity of autism measurements could be explained, in part, by regression analyses of urinary excretion of toxic metals before and after DMSA and the level of RBC glutathione (adjusted in all cases). This study demonstrates a significant positive association between the severity of autism and the relative body burden of toxic metals.http://www.hindawi.com/journals/jt/2009/532640/ Oxidative Stress Causes Renal Dopamine D1 Receptor Dysfunction and Hypertension via Mechanisms That Involve Nuclear Factor-κB and Protein Kinase Chttp://jasn.asnjournals.org/content/18/5/1446.long Low natural killer cell cytotoxic activity in autism: The role of glutathione, IL-2 and IL-15http://www.sciencedirect.com/science/article/pii/S0165572808003986 Oxidative stress in autism NYS Institute for Basic Research in Developmental Disabilities Excerpt: Several studies have suggested alterations in the activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and catalase in autism. Additionally, altered glutathione levels and homocysteine/methionine metabolism, increased inflammation, excitotoxicity, as well as mitochondrial and immune dysfunction have been suggested in autismhttp://www.sciencedirect.com/science/article/pii/S0928468006000538 Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism Excerpt: These results suggest that the autism LCLs exhibit a reduced glutathione reserve capacity in both cytosol and mitochondria that may compromise antioxidant defense and detoxification capacity under prooxidant conditions.http://www.fasebj.org/content/23/8/2374.short Neurotoxicology. 2005 Jan;26(1):1-8. Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors.http://www.ncbi.nlm.nih.gov/pubmed/15527868 Induction of Oxidative Stress by Glutathione Depletion Causes Severe Hypertension in Normal Ratshttp://www.ncbi.nlm.nih.gov/pubmed/10904027http://hyper.ahajournals.org/content/36/1/142.full.pdfhttp://ndt.oxfordjournals.org/content/18/8/1439.full.pdf

————————– Brain Res. 2006 Oct 20;1116(1):215-21. Epub 2006 Aug 30. Aluminum complexing enhances amyloid beta protein penetration of blood-brain barrier. Banks WA, Niehoff ML, Drago D, Zatta P. Source:GRECC, Veterans Affairs Medical Center-St. Louis and Saint Louis University School of Medicine, Division of Geriatrics, Department of Internal Medicine, WAB, 915 N. Grand Blvd, St. Louis, MO 63106, USA. Abstract A significant co-morbidity of Alzheimer’s disease and cerebrovascular impairment suggests that cerebrovascular dysregulation is an important feature of dementia. Amyloid beta protein (Abeta), a relevant risk factor in Alzheimer’s disease, has neurotoxic properties and is thought to play a critical role in the cognitive impairments. Previously, we demonstrated that the 42mer of Abeta (Abeta42) complexed with aluminum (Al-Abeta42) is much more cytotoxic than non-complexed Abeta42. The level of Abeta in the brain is a balance between synthesis, degradation, and fluxes across the blood-brain barrier (BBB). In the present paper, we determined whether complexing with aluminum affected the ability of radioactively iodinated Abeta to cross the in vivo BBB. We found that the rates of uptake of Al-Abeta42 and Abeta42 were similar, but that Al-Abeta42 was sequestered by brain endothelial cells much less than Abeta42 and so more readily entered the parenchymal space of the brain. Al-Abeta42 also had a longer half-life in blood and had increased permeation at the striatum and thalamus. Brain-to-blood transport was similar for Al-Abeta42 and Abeta42. In conclusion, complexing with aluminum affects some aspects of blood-to-brain permeability so that Al-Abeta42 would have more ready access to brain cells than Abeta42.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/16942756 ——————– General listings of aluminum related abstracts in Pubmed J Cell Biochem. 2004 Dec 15;93(6):1267-71. Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria. Murakami K, Yoshino M. Source Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.http://www.ncbi.nlm.nih.gov/pubmed/15486972 Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondriahttp://onlinelibrary.wiley.com/doi/10.1002/jcb.20261/abstract ———————-- Expert Rev Clin Immunol. 2010 May;6(3):397-411. Autism spectrum disorders and allergy: observation from a pediatric allergy/immunology clinic.http://www.ncbi.nlm.nih.gov/pubmed/20441426 ———————-- Mult Scler. 2006 Oct;12(5):533-40. Elevated urinary excretion of aluminium and iron in multiple sclerosis. Exley C, Mamutse G, Korchazhkina O, Pye E, Strekopytov S, Polwart A, Hawkins C. Source:Birchall Centre for Inorganic Chemistry and Materials Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK. c.exley@chem.keele.ac.uk Abstract Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system of as yet unknown aetiology. A consensus of opinion has suggested that the disorder is the result of an interplay between environmental factors and susceptibility genes. We have used a battery of analytical techniques to determine if the urinary excretion of i) markers of oxidative damage; ii) iron and iii) the environmental toxin aluminium and its antagonist, silicon, are altered in relapsing-remitting (RRMS) and secondary progressive MS (SPMS). Urinary concentrations of oxidative biomarkers, MDA and TBARS, were not found to be useful indicators of inflammatory disease in MS. However, urinary concentrations of another potential marker for inflammation and oxidative stress, iron, were significantly increased in SPMS (P<0.01) and insignificantly increased in RRMS (P>0.05). Urinary concentrations of aluminium were also significantly increased in RRMS (P<0.001) and SPMS (P <0.05) such that the levels of aluminium excretion in the former were similar to those observed in individuals undergoing metal chelation therapy. The excretion of silicon was lower in MS and significantly so in SPMS (P<0.05). Increased excretion of iron in urine supported a role for iron dysmetabolism in MS. Levels of urinary aluminium excretion similar to those seen in aluminium intoxication suggested that aluminium may be a hitherto unrecognized environmental factor associated with the aetiology of MS. If aluminium is involved in MS then an increased dietary intake of its natural antagonist, silicon, might be a therapeutic option.http://www.ncbi.nlm.nih.gov/pubmed/17086897 —————– J Inorg Biochem. 2007 Sep;101(9):1275-84. Epub 2007 Jun 12. An aluminum-based rat model for Alzheimer’s disease exhibits oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and granulovacuolar degeneration. Walton JR. Source: Australian Institute for Biomedical Research, Sydney, NSW, Australia. Abstract In Alzheimer’s disease (AD), oxidative damage leads to the formation of amyloid plaques while low PP2A activity results in hyperphosphorylated tau that polymerizes to form neurofibrillary tangles. We probed these early events, using brain tissue from a rat model for AD that develops memory deterioration and AD-like behaviors in old age after chronically ingesting 1.6 mg aluminum/kg bodyweight/day, equivalent to the high end of the human dietary aluminum range. A control group consumed 0.4 mg aluminum/kg/day. We stained brain sections from the cognitively-damaged rats for evidence of amyloid plaques, neurofibrillary tangles, aluminum, oxidative damage, and hyperphosphorylated tau. PP2A activity levels measured 238.71+/-17.56 pmol P(i)/microg protein and 580.67+/-111.70 pmol P(i)/microg protein (p<0.05) in neocortical/limbic homogenates prepared from cognitively-damaged and control rat brains, respectively. Thus, PP2A activity in cognitively-damaged brains was 41% of control value. Staining results showed: (1) aluminum-loading occurs in some aged rat neurons as in some aged human neurons; (2) aluminum-loading in rat neurons is accompanied by oxidative damage, hyperphosphorylated tau, neuropil threads, and granulovacuolar degeneration; and (3) amyloid plaques and neurofibrillary tangles were absent from all rat brain sections examined. Known species difference can reasonably explain why plaques and tangles are unable to form in brains of genetically-normal rats despite developing the same pathological changes that lead to their formation in human brain. As neuronal aluminum can account for early stages of plaque and tangle formation in an animal model for AD, neuronal aluminum could also initiate plaque and tangle formation in humans with AD.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/17662457 KURODA, Y. and KAWAHARA, M. Aggregation of Amyloid -Protein and Its Neurotoxicity: Enhancement by Aluminum and Other Metals.http://www.ncbi.nlm.nih.gov/pubmed/7761991 Brain Res Bull. 2001 May 15;55(2):211-7. Effects of aluminum on the neurotoxicity of primary cultured neurons and on the aggregation of beta-amyloid protein. Kawahara M, Kato M, Kuroda Y.http://www.ncbi.nlm.nih.gov/pubmed/11470317 —————– Toxicol In Vitro. 2007 Feb;21(1):16-24. Epub 2006 Aug 5. Aluminum toxicity triggers the nuclear translocation of HIF-1alpha and promotes anaerobiosis in hepatocytes. Mailloux RJ, Appanna VD. Source:Department of Chemistry and Biochemistry, Laurentian University, Sudbury, Ont., Canada P3E 2C6. Excerpted: HPLC analyses confirmed increased glycolytic ATP production in Al-exposed hepatocytes. These findings reveal the ability of Al to create a hypoxic environment that promotes the translocation of HIF-1alpha to the nucleus and stimulates the anaerobic metabolism of D-glucose. —————– J Trace Elem Med Biol. 2001;15(2-3):139-41. Inhibitory effect of aluminum on dopamine beta-hydroxylase from bovine adrenal gland. Excerpt: Aluminum is a well known neurotoxic agent that is overaccumulated in the substantia nigra of patients affected by Parkinson’s disease as well as in certain cerebral areas of other neurodegenerative pathologies such as Alzheimer’s disease. Although the role of aluminum in neurodegenerative diseases is yet to be clearly understood, the metal ion is known to substantially alter the activity of several key enzymes in the central nervous system. The potential implications of aluminum in the etiopathogenesis of neurological disorders are discussed.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/11787979 ————- [Toxic effects of aluminum on human embryonic cerebral neurocytes in vitro studies]. Huang G, Kang J, Zhang W, Liu L, Yu M, Mei M, Dong Y. Excerpt: CONCLUSIONS: The growth, development and function of human embryonic cerebral neurocytes was inhibited in the high Al group. The neurotoxicity of Al may be caused by lipid peroxidation and the damage of cell membrane.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/11860913 ————– J Inorg Biochem. 2003 Sep 15;97(1):132-42. Aluminium-induced impairment of Ca2+ modulatory action on GABA transport in brain cortex nerve terminals. Cordeiro JM, Silva VS, Oliveira CR, Gonçalves PP. Source:Centre for Environmental and Marine Studies, Department of Biology, University of Aveiro, 3810-193 Aveiro, Portugal. Excerpt: In conclusion, aluminium-induced relief of Ca(2+) modulatory action on GABA transporter may contribute significantly to modify GABAergic signalling during neurotoxic events in response to aluminium exposure.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/14507469 ————-- J Biochem Mol Toxicol. 2006;20(4):198-208. Aluminum toxicity elicits a dysfunctional TCA cycle and succinate accumulation in hepatocytes. Mailloux RJ, Hamel R, Appanna VD. Source:Department of Chemistry and Biochemistry, Laurentian University, Sudbury, Ontario, Canada, P3E 2C6. In conclusion, these results suggest that Al toxicity promotes a dysfunctional TCA cycle and impedes ATP production, events that may contribute to various Al-induced abnormalities.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/16906525 ————-- Aluminum modulates brain amyloidosis through oxidative stress in APP transgenic mice. Praticò D, Uryu K, Sung S, Tang S, Trojanowski JQ, Lee VM. Source: Center for Experimental Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania Excerpt: These results indicate that dietary Al can modulate in vivo AD-like amyloidosis in Tg2576 by increasing brain oxidative stress. Toxicol Ind Health. 2006 Feb;22(1):39-46. Possible peripheral markers for chronic aluminium toxicity in Wistar rats. Kaur A, Gill KD. Source:Department of Biochemistry, Post Graduate Institute of Medical Education and Research, Chandigarh, India. Abstract This investigation gives detailed analysis of peripheral marker enzymes as well as neurobehavioral tests following chronic aluminium (Al) exposure (10 mg/kg b.w. for 12 weeks intragastrically). We observed a significant decrease in the levels of serum cholinesterase after toxicity. The enzymatic activity of cytochrome oxidase (CO), the terminal enzyme of the electron transport chain, was significantly diminished and that of glucose-6-phosphate dehydrogenase (G-6-PD) was significantly enhanced. Neuromuscular co-ordination was assessed using motor and memory function tests. Deficits were observed suggesting a probable model for chronic Al neurotoxicity.http://www.ncbi.nlm.nih.gov/pubmed/16572710 ——————————–

Same mechanisms of action in relation to needed necessary glutathione as to detoxification of both mercury and aluminum. J Cell Biochem. 2004 Dec 15;93(6):1267-71. Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria. Murakami K, Yoshino M. Source:Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan. Abstract Effect of aluminum on the NADPH supply and glutathione regeneration in mitochondria was analyzed. Reduced glutathione acted as a principal scavenger of reactive oxygen species in mitochondria. Aluminum inhibited the regeneration of glutathione from the oxidized form, and the effect was due to the inhibition of NADP-isocitrate dehydrogenase the only enzyme supplying NADPH in mitochondria. In cytosol, aluminum inhibited the glutathione regeneration dependent on NADPH supply by malic enzyme and NADP-isocitrate dehydrogenase, but did not affect the glucose 6-phosphate dehydrogenase dependent glutathione formation. Aluminum can cause oxidative damage on cellular biological processes by inhibiting glutathione regeneration through the inhibition of NADPH supply in mitochondria, but only a little inhibitory effect on the glutathione generation in cytosol.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/15486972 ——————————– J Enzyme Inhib Med Chem. 2004 Aug;19(4):317-25. The effect of cations on the amidase activity of human tissue kallikrein: 1-linear competitive inhibition by sodium, potassium, calcium and magnesium. 2-linear mixed inhibition by aluminium. De Sousa MO, Santoro MM, De Souza Figueiredo AF. Source:Departamento de Análises Clínicas e Toxicológicas, Faculdade de Farmácia, Universidade Federal de Minas Gerais, C. P. 689, 30123-970 Belo Horizonte, MG, Brazil. Excerpt: Aluminium is not a physiological cation, but is a known neurotoxicant for animals and humans. The neurotoxic actions of aluminium may relate to neuro-degenerative diseases.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/15558947 ——————————– Proc Soc Exp Biol Med. 2000 Apr;223(4):397-402. Aluminum increases levels of beta-amyloid and ubiquitin in neuroblastoma but not in glioma cells. Excerpted: These data suggest that one of the mechanisms by which Al may play a role in AD is by promoting the formation of Abeta and ubiquitin in neurons.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/10721010

Vaccination Hazards - Nanobacteria + some additives in vaccines are extremely harmful. (Vaccine contamination is an unresolved problem regardless of the established step process and both the CDC and FDA know that, in review their documents; yet they whitewash it with the public, claiming there is no evidence nor scientific proof proof of the harm. Yet, it is obvious that they know of the risk to human health that vaccine contamination can cause. Liars. The present concerns about mandatory vaccinations under the Homeland Security Act are well founded. What has not been understood is the method of action that causes vaccination toxicity. The following is a simplification of the underlying cause, method of action and remedial measures to reduce the damage with references. Note that the medical reviews in journals and on the web belittle the anti-vaccination sites as based only on emotion, etc. 1. The introduction of any bacteria or bacterial filtrate alive or dead ( vaccine ) causes a reaction of the body that results in blood clots from intense microbial action. These clots may be small adhesions that attach to the blood vessels or organs impairing their function or complete obstructions resulting in organ death. They are particularly common in kidney, lung, liver and brain. This intravascular coagulation is readily apparent in an examination of the blood vessels in the sclera ( whites ) of the eyes from vaccines. This is known as the Sarannelli / Schwartzman phenomena. There are several hundred references to its occurrence in the National Library of Medicine. It is called phenomena because the cause has not been understood. 2. Intense microbial action ( infection ) or microbial agents cause a reduction in zeta potential* which changes blood to "sludge." 3. The administration of more than one vaccine at a time multiplies the effect increasing the amount of intravascular coagulation and blood clots. 4. The use of aluminum salts to stabilize vaccines exacerbates the effect by a multiple of 6,000 times. By making a flour-water mixture and adding a drop of deodorant one can easily observe the coagulation effect of aluminum. The flour will immediately clump and settle to the bottom. As an alternative, rub oil on the arm and apply a small amount of deodorant. The oil will immediately coagulate and roll up in little balls. Aluminum is the primary ingredient in most antiperspirants as it causes the sweat to coagulate and block the pores in sweat glands. 5. There are over 7,000 references to the toxicity of aluminum. http://www.luminet.net/~wenonah/hydro/al.htm#toxic

The alternative non pharma connected journals are just full of these kind of studies, and as well is Pubmed. The only science the CDC allows to be represented of course is what they cherry pick and fund themselves. We have been lied to, and someone is obviously and intentionally asleep at the research library at the CDC. To much to lose, if the truth be known on a large scale, and especially if they had to admit to it publicly.

This next one was listed above, but could that be more important, this finding. Why are they still using aluminum adjuvants? And the new designer adjuvants are causing just as many if not more problems, and potential problems. Aluminium in vaccines can cause serious polio-like damage, damage motorneuron cells and cause brain damage – possibly leading to Alzheimer’s and other forms of dementia and increasing the risk in children of Autistic Spectrum Disorders. From the Transcripts of the US Vaccines and Related Biological Advisory Committee Meeting (VRBAC) and Scientific Papers The Experts admitted Ignorancehttp://albamora.com/joanmorahomeopatia/pdf/Aluminum%20in%20Vaccines%20-from%20forthcoming%20book.pdf ASD and Aluminum Toxicityhttp://drtenpenny.com/Documents/Aluminum%20part%202%20(157%20slide).pdf -------------------------- General listing of aluminum related abstracts in Pubmed Brain Res. 2006 Oct 20;1116(1):215-21. Epub 2006 Aug 30. Aluminum complexing enhances amyloid beta protein penetration of blood-brain barrier. Banks WA, Niehoff ML, Drago D, Zatta P. Source:GRECC, Veterans Affairs Medical Center-St. Louis and Saint Louis University School of Medicine, Division of Geriatrics, Department of Internal Medicine, WAB, 915 N. Grand Blvd, St. Louis, MO 63106, USA. Abstract A significant co-morbidity of Alzheimer's disease and cerebrovascular impairment suggests that cerebrovascular dysregulation is an important feature of dementia. Amyloid beta protein (Abeta), a relevant risk factor in Alzheimer's disease, has neurotoxic properties and is thought to play a critical role in the cognitive impairments. Previously, we demonstrated that the 42mer of Abeta (Abeta42) complexed with aluminum (Al-Abeta42) is much more cytotoxic than non-complexed Abeta42. The level of Abeta in the brain is a balance between synthesis, degradation, and fluxes across the blood-brain barrier (BBB). In the present paper, we determined whether complexing with aluminum affected the ability of radioactively iodinated Abeta to cross the in vivo BBB. We found that the rates of uptake of Al-Abeta42 and Abeta42 were similar, but that Al-Abeta42 was sequestered by brain endothelial cells much less than Abeta42 and so more readily entered the parenchymal space of the brain. Al-Abeta42 also had a longer half-life in blood and had increased permeation at the striatum and thalamus. Brain-to-blood transport was similar for Al-Abeta42 and Abeta42. In conclusion, complexing with aluminum affects some aspects of blood-to-brain permeability so that Al-Abeta42 would have more ready access to brain cells than Abeta42.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/16942756 -------------------- J Cell Biochem. 2004 Dec 15;93(6):1267-71. Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria. Murakami K, Yoshino M. Source Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.http://www.ncbi.nlm.nih.gov/pubmed/15486972 Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondriahttp://onlinelibrary.wiley.com/doi/10.1002/jcb.20261/abstract ------------------------ Mult Scler. 2006 Oct;12(5):533-40. Elevated urinary excretion of aluminium and iron in multiple sclerosis. Exley C, Mamutse G, Korchazhkina O, Pye E, Strekopytov S, Polwart A, Hawkins C. Source:Birchall Centre for Inorganic Chemistry and Materials Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK. c.exley@chem.keele.ac.uk Abstract Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system of as yet unknown aetiology. A consensus of opinion has suggested that the disorder is the result of an interplay between environmental factors and susceptibility genes. We have used a battery of analytical techniques to determine if the urinary excretion of i) markers of oxidative damage; ii) iron and iii) the environmental toxin aluminium and its antagonist, silicon, are altered in relapsing-remitting (RRMS) and secondary progressive MS (SPMS). Urinary concentrations of oxidative biomarkers, MDA and TBARS, were not found to be useful indicators of inflammatory disease in MS. However, urinary concentrations of another potential marker for inflammation and oxidative stress, iron, were significantly increased in SPMS (P<0.01) and insignificantly increased in RRMS (P>0.05). Urinary concentrations of aluminium were also significantly increased in RRMS (P<0.001) and SPMS (P <0.05) such that the levels of aluminium excretion in the former were similar to those observed in individuals undergoing metal chelation therapy. The excretion of silicon was lower in MS and significantly so in SPMS (P<0.05). Increased excretion of iron in urine supported a role for iron dysmetabolism in MS. Levels of urinary aluminium excretion similar to those seen in aluminium intoxication suggested that aluminium may be a hitherto unrecognized environmental factor associated with the aetiology of MS. If aluminium is involved in MS then an increased dietary intake of its natural antagonist, silicon, might be a therapeutic option.http://www.ncbi.nlm.nih.gov/pubmed/17086897 ----------------- J Inorg Biochem. 2007 Sep;101(9):1275-84. Epub 2007 Jun 12. An aluminum-based rat model for Alzheimer's disease exhibits oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and granulovacuolar degeneration. Walton JR. Source: Australian Institute for Biomedical Research, Sydney, NSW, Australia. Abstract In Alzheimer's disease (AD), oxidative damage leads to the formation of amyloid plaques while low PP2A activity results in hyperphosphorylated tau that polymerizes to form neurofibrillary tangles. We probed these early events, using brain tissue from a rat model for AD that develops memory deterioration and AD-like behaviors in old age after chronically ingesting 1.6 mg aluminum/kg bodyweight/day, equivalent to the high end of the human dietary aluminum range. A control group consumed 0.4 mg aluminum/kg/day. We stained brain sections from the cognitively-damaged rats for evidence of amyloid plaques, neurofibrillary tangles, aluminum, oxidative damage, and hyperphosphorylated tau. PP2A activity levels measured 238.71+/-17.56 pmol P(i)/microg protein and 580.67+/-111.70 pmol P(i)/microg protein (p<0.05) in neocortical/limbic homogenates prepared from cognitively-damaged and control rat brains, respectively. Thus, PP2A activity in cognitively-damaged brains was 41% of control value. Staining results showed: (1) aluminum-loading occurs in some aged rat neurons as in some aged human neurons; (2) aluminum-loading in rat neurons is accompanied by oxidative damage, hyperphosphorylated tau, neuropil threads, and granulovacuolar degeneration; and (3) amyloid plaques and neurofibrillary tangles were absent from all rat brain sections examined. Known species difference can reasonably explain why plaques and tangles are unable to form in brains of genetically-normal rats despite developing the same pathological changes that lead to their formation in human brain. As neuronal aluminum can account for early stages of plaque and tangle formation in an animal model for AD, neuronal aluminum could also initiate plaque and tangle formation in humans with AD.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/17662457 KURODA, Y. and KAWAHARA, M. Aggregation of Amyloid -Protein and Its Neurotoxicity: Enhancement by Aluminum and Other Metals.http://www.ncbi.nlm.nih.gov/pubmed/7761991 Brain Res Bull. 2001 May 15;55(2):211-7. Effects of aluminum on the neurotoxicity of primary cultured neurons and on the aggregation of beta-amyloid protein. Kawahara M, Kato M, Kuroda Y.http://www.ncbi.nlm.nih.gov/pubmed/11470317 ----------------- Toxicol In Vitro. 2007 Feb;21(1):16-24. Epub 2006 Aug 5. Aluminum toxicity triggers the nuclear translocation of HIF-1alpha and promotes anaerobiosis in hepatocytes. Mailloux RJ, Appanna VD. Source:Department of Chemistry and Biochemistry, Laurentian University, Sudbury, Ont., Canada P3E 2C6. Excerpted: HPLC analyses confirmed increased glycolytic ATP production in Al-exposed hepatocytes. These findings reveal the ability of Al to create a hypoxic environment that promotes the translocation of HIF-1alpha to the nucleus and stimulates the anaerobic metabolism of D-glucose. ----------------- J Trace Elem Med Biol. 2001;15(2-3):139-41. Inhibitory effect of aluminum on dopamine beta-hydroxylase from bovine adrenal gland. Excerpt: Aluminum is a well known neurotoxic agent that is overaccumulated in the substantia nigra of patients affected by Parkinson's disease as well as in certain cerebral areas of other neurodegenerative pathologies such as Alzheimer's disease. Although the role of aluminum in neurodegenerative diseases is yet to be clearly understood, the metal ion is known to substantially alter the activity of several key enzymes in the central nervous system. The potential implications of aluminum in the etiopathogenesis of neurological disorders are discussed.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/11787979 -------------Toxic effects of aluminum on human embryonic cerebral neurocytes in vitro studies. Huang G, Kang J, Zhang W, Liu L, Yu M, Mei M, Dong Y. Excerpt: CONCLUSIONS: The growth, development and function of human embryonic cerebral neurocytes was inhibited in the high Al group. The neurotoxicity of Al may be caused by lipid peroxidation and the damage of cell membrane.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/11860913 -------------- J Inorg Biochem. 2003 Sep 15;97(1):132-42. Aluminium-induced impairment of Ca2+ modulatory action on GABA transport in brain cortex nerve terminals. Cordeiro JM, Silva VS, Oliveira CR, Gonçalves PP. Source:Centre for Environmental and Marine Studies, Department of Biology, University of Aveiro, 3810-193 Aveiro, Portugal. Excerpt: In conclusion, aluminium-induced relief of Ca(2+) modulatory action on GABA transporter may contribute significantly to modify GABAergic signalling during neurotoxic events in response to aluminium exposure.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/14507469 --------------- J Biochem Mol Toxicol. 2006;20(4):198-208. Aluminum toxicity elicits a dysfunctional TCA cycle and succinate accumulation in hepatocytes. Mailloux RJ, Hamel R, Appanna VD. Source:Department of Chemistry and Biochemistry, Laurentian University, Sudbury, Ontario, Canada, P3E 2C6. In conclusion, these results suggest that Al toxicity promotes a dysfunctional TCA cycle and impedes ATP production, events that may contribute to various Al-induced abnormalities.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/16906525 --------------- Aluminum modulates brain amyloidosis through oxidative stress in APP transgenic mice. Praticò D, Uryu K, Sung S, Tang S, Trojanowski JQ, Lee VM. Source: Center for Experimental Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania Excerpt: These results indicate that dietary Al can modulate in vivo AD-like amyloidosis in Tg2576 by increasing brain oxidative stress. Toxicol Ind Health. 2006 Feb;22(1):39-46. Possible peripheral markers for chronic aluminium toxicity in Wistar rats. Kaur A, Gill KD. Source:Department of Biochemistry, Post Graduate Institute of Medical Education and Research, Chandigarh, India. Abstract This investigation gives detailed analysis of peripheral marker enzymes as well as neurobehavioral tests following chronic aluminium (Al) exposure (10 mg/kg b.w. for 12 weeks intragastrically). We observed a significant decrease in the levels of serum cholinesterase after toxicity. The enzymatic activity of cytochrome oxidase (CO), the terminal enzyme of the electron transport chain, was significantly diminished and that of glucose-6-phosphate dehydrogenase (G-6-PD) was significantly enhanced. Neuromuscular co-ordination was assessed using motor and memory function tests. Deficits were observed suggesting a probable model for chronic Al neurotoxicity.http://www.ncbi.nlm.nih.gov/pubmed/16572710 -------------------------------- J Cell Biochem. 2004 Dec 15;93(6):1267-71. Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria. Murakami K, Yoshino M. Source:Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan. Abstract Effect of aluminum on the NADPH supply and glutathione regeneration in mitochondria was analyzed. Reduced glutathione acted as a principal scavenger of reactive oxygen species in mitochondria. Aluminum inhibited the regeneration of glutathione from the oxidized form, and the effect was due to the inhibition of NADP-isocitrate dehydrogenase the only enzyme supplying NADPH in mitochondria. In cytosol, aluminum inhibited the glutathione regeneration dependent on NADPH supply by malic enzyme and NADP-isocitrate dehydrogenase, but did not affect the glucose 6-phosphate dehydrogenase dependent glutathione formation. Aluminum can cause oxidative damage on cellular biological processes by inhibiting glutathione regeneration through the inhibition of NADPH supply in mitochondria, but only a little inhibitory effect on the glutathione generation in cytosol.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/15486972 -------------------------------- J Enzyme Inhib Med Chem. 2004 Aug;19(4):317-25. The effect of cations on the amidase activity of human tissue kallikrein: 1-linear competitive inhibition by sodium, potassium, calcium and magnesium. 2-linear mixed inhibition by aluminium. De Sousa MO, Santoro MM, De Souza Figueiredo AF. Source:Departamento de Análises Clínicas e Toxicológicas, Faculdade de Farmácia, Universidade Federal de Minas Gerais, C. P. 689, 30123-970 Belo Horizonte, MG, Brazil. Excerpt: Aluminium is not a physiological cation, but is a known neurotoxicant for animals and humans. The neurotoxic actions of aluminium may relate to neuro-degenerative diseases.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/15558947 -------------------------------- Proc Soc Exp Biol Med. 2000 Apr;223(4):397-402. Aluminum increases levels of beta-amyloid and ubiquitin in neuroblastoma but not in glioma cells. Excerpted: These data suggest that one of the mechanisms by which Al may play a role in AD is by promoting the formation of Abeta and ubiquitin in neurons.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/10721010 ------------------------------ Biochemistry (Mosc). 2006 Mar;71(3):239-44. Effects of vitamin E against aluminum neurotoxicity in rats. Nedzvetsky VS, Tuzcu M, Yasar A, Tikhomirov AA, Baydas G. Source:Department of Biophysics and Biochemistry, Faculty of Biology, Dnepropetrovsk National University, Ukraine. Abstract The present study examined the protective effects of vitamin E against aluminum-induced neurotoxicity in rats. Wistar rats were given daily aluminum via their drinking water containing 1600 mg/liter aluminum chloride for six weeks. Aluminum induced a significant increase in lipid peroxidation (LPO) in hippocampus and frontal cortex. Furthermore, aluminum caused marked elevation in the levels of the glial markers (glial fibrillary acidic protein (GFAP) and S100B) and proinflammatory cytokines (TNF-alpha and IL-1beta) in both brain areas. Vitamin E treatment reduced the contents of glial markers and cytokines and the levels of LPO. In conclusion, this study demonstrates that vitamin E ameliorates glial activation and reduces release of proinflammatory cytokines induced by aluminum.http://0-www.ncbi.nlm.nih.gov.opac.acc.msmc.edu/pubmed/16545059 ---------------------------------------- Conference report - (A CDC connected document) Workshop summary Aluminum in vaccines My remarks are marked with and by [...] A discussion of the increase in antibody production in the use of adjuvanted vaccines. A claim is made in the article, exceprted below. Some excerpts from the article: The ﬁrst panel identiﬁed the following facts that are known about aluminum in vaccines. 6. More data is needed on the toxicopharmacology of aluminum exposures by the IM route; however, there appears to be little potential for toxicity with vaccine-level exposures to aluminum. [There is however very limited data, and there are NO human safety studies listed, to support that claim.] The second panel discussed “what we don’t know” about aluminum-containing adjuvants and identiﬁed the followingareas to be more thoroughly studied. 1. Toxicology and pharmacokinetics of aluminum adjuvants. Speciﬁcally, the processing of aluminum by infants and children. 2. Mechanisms by which aluminum adjuvants interact with the immune system. 4. Deﬁnition of frequency and duration of the MMF lesion in normal people. 5. Role of aluminum in the pathophysiology of the MMF lesion. 6. Human control studies to assess the relationship between the “symptom complex” identiﬁed by Dr. Gherardi in patients who have the MMF lesion and the MMF lesion The newly recognized histologic entity, MMF, was originally described in France in 1993, and ﬁrst published in 1998 (Lancet 352 (1998) 347–352). In his presentation, Dr. Gherardi stated that there have been 100 cases collected so far, 92 of which are from France. The observations that he presented were derived from the ﬁrst 50 such patients. Deltoid muscle biopsies in those individuals revealed an unusual pattern of extensive inﬁltration of macrophages around, but not inside, muscle ﬁbers. There were also a few CD8+ T cells. Many of the macrophages were noted to contain PAS-positive crystalline structures, which subsequently were identiﬁed as aluminum salts. Notably there was not muscle ﬁber damage, necrosis, giant cells, nor mitotic ﬁgures. Dr. Gherardi also noted among these patients a cluster of symptoms consisting of diffuse myalgia, arthralgia,and fatigue. Laboratory evidence of inﬂammation was variable; most patients had a normal white blood count, but about half had some serum autoantibodies present. In addition, serum levels of certain cytokines seemed to be significantly increased, particularly IL-1 receptor antagonist and IL-6.These patients were mostly middle-age adults with males and females about equally represented. All of them had received aluminum-containing vaccines, mostly hepatitis B vaccine, presumably in the biopsied deltoid muscle. Source:http://archive.hhs.gov/nvpo/nvac/documents/Aluminumws.pdf This said article goes on to make the following claims: Each individual has a molecular level of protective response to toxins. One of the cellular level protective mechanism is the formation of metallo-thionine complexes, capable of binding many metals, such as mercury but not aluminum There is no data on the potential toxicity of the mixture of mercury and aluminum. Discussion focused on the desirability of identifying possible biomarkers for toxicity. Session II was led off by Dr. Stanley Hem, of Purdue University. He discussed the pharmacology of aluminum salts, and introduced the workshop participants to just how much aluminum we are exposed to, how much is in us, and howit is handled within the body. An average daily exposure is about 10–15 mg, most of which comes from foods. While aluminum adjuvants have been used in vaccines for many years, their disposition following intramuscular (IM) administration has not been studied because the low dose did not cause detectable changes in the normal plasma concentration (5g aluminum/l). Now, accelerator mass spectrometry (AMS) can accurately measure very small concentrations(10−17 g) of aluminum 26 which has no measurable radiation and is considered safe. Preliminary animal experiments have shown that the aluminum adjuvants are dissolved by citrate in the interstitial ﬂuid, leaving the body rapidly. The ability of the body to eliminate aluminum-containing adjuvants may be partly responsible for the excellent safety record of these adjuvants. [So, here we have it, aluminum is safe because it contains no radiation??? Why didn't they at least list the animals studies? Nothing. How do they know aluminum left the body rapidly? And there was what done to determine how much was left in the brain, etc.? Did they autopsy the animals? Did they do any live blood cell blood microscopy, to see what actually happened in the blood, after injection of an aluminum adjuvant? Nope, obviously not. Excellent safety record? Based on what, that the subjects didn't die on the spot, after injection?] Drs. Sam Keith and John Wheeler, both of the Agency for Toxic Substances and Disease Registry (ASTDR), discussed aluminum toxicology and minimum risk levels. These were particularly helpful presentations both in understanding the ubiquity of aluminum in our environment (aluminum is our third most abundant element behind oxygen and silicon), and understanding the uncertainties incorporated into establishing guidance levels. There seems to be abundant dataconcerning risk levels for ingested aluminum, but scant data about risk levels for injected aluminum. The oral minimum risk level, for example, appears to be in the range of 2–60 mg/kg of aluminum per day but there are no comparable data for injected aluminum. The uncertainties notwithstanding, there appeared to be a large margin of safety for aluminum adjuvants [Wow, so that is conclusive; its all good, safe and effective? Without any actual data?]

Hum Exp Toxicol. 2012 October; 31(10): 1012–1021.PMCID: PMC3547435 Relative trends in hospitalizations and mortality among infants by the number of vaccine doses and age, based on the Vaccine Adverse Event Reporting System (VAERS), 1990–2010 GS Goldman1 and NZ Miller2 Conclusion VAERS is one of the largest databases containing adverse reactions reported in temporal association with vaccination. While some adverse events that are reported to VAERS may be unrelated to the recent vaccination, the VAERS database is an important postmarketing safety surveillance tool that is periodically analyzed by the CDC, FDA, and other vaccine researchers to discover potentially adverse vaccination trends. Using linear regression, several statistically significant trends were derived from the VAERS database: (a) a positive correlation between hospitalization rates and the number of vaccine doses (r 2 = 0.91); (b) a negative correlation between hospitalization rates and age (r 2 = 0.95); (c) an increased mortality rate associated with 5–8 vaccines relative to 1–4 vaccines; (d) a decreased mortality rate associated with children aged 0.5 to <1 year relative to those aged <0.5 year; and (e) a 1.4 male-to-female infant mortality ratio. These trends not only have a biological plausibility but are supported by evidence from case reports, case series, and other studies using entirely different methodologies and specific population cohorts. Studies have not been conducted to determine the safety (or efficacy) of administering multiple vaccine doses in a variety of combinations as recommended by CDC guidelines. Our findings show a positive correlation between the number of vaccine doses administered and the percentage of hospitalizations and deaths reported to VAERS. In addition, younger infants were significantly more likely than older infants to be hospitalized or die after receiving vaccines. Since vaccines are administered to millions of infants every year, it is imperative that health authorities have scientific data from synergistic toxicity studies on all combinations of vaccines that infants are likely to receive; universal vaccine recommendations must be supported by such studies. Adverse reaction trends detected in VAERS have important implications for vaccine recipients and health care providers. Finding ways to increase vaccine safety should be the highest priority. Further inspection of potential correlations between increasing vaccine doses, hospitalizations, and death is essential. Health care policy makers have an obligation to determine whether immunization schedules are achieving their desired goals.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3547435/And would or should any person need to see or know, anymore? Vaccines, MORE harm than good!

It, this situation, has been going on for the past 100 years, and only getting worse. The whole foundation of modern medicine was built on the incorrect premises promoted by Pasteur. The false germ theory, the soil and the seed. There is a clear reason it all is like it is. Money, greed, and profit. Bechamp's well proven, (more than a theory), would never have sold millions in chemical based pharma drugs and vaccines. To use Bechamp's principals, would effect a true understanding of the cause, and true healing. Everything in the naturopathic was falsely railed on as unproven quackery, while the real quackery they claimed was science based, and the only thing in a medical school that would accepted. We have the Rockefellers and their early oil money to thank for it all, and the way it yet stands today; and The Flexner Report. This is all easily researchable and verified. When you even have the power to buy the Encyclopedia Brittanica and remove what you do not want in it, essentially rewriting history, then you as well have the total control to decieve the masses, and no one is supposed to be the wiser. Look at the good job they did of it? How many people actually realize that this is why it all remains in the failed situation it is within the medical establishment? They will yet deny that it is and has failed. Nothing would quite obviously ever be enough to get them to face it; as they simply have to much to lose. They are not losing their billion dollar market, pharma vaccines; nor their careers, to change it now. Nor will they allow themselves to be liable for generations of vaccine harm. And it is only getting worse. Louis Pasteur vs. Antoine Bechamp: Know the True Causes of Diseasehttp://www.naturalnews.com/030384_Louis_Pasteur_disease.htmlLouis Pasteur Vs Antoine Béchamp and The Germ Theory of Disease Causation - 1 Excerpts: We do not catch diseases. We build them. We have to eat, drink, think, and feel them into existence. We work hard at developing our diseases. We must work just as hard at restoring health. The presence of germs does not constitute the presence of a disease. Bacteria are scavengers of nature...they reduce dead tissue to its smallest element. Germs or bacteria have no influence, whatsoever, on live cells. Germs or microbes flourish as scavengers at the site of disease. They are just living on the unprocessed metabolic waste and diseased, malnourished, nonresistant tissue in the first place. They are not the cause of the disease, any more than flies and maggots cause garbage. Flies, maggots, and rats do not cause garbage but rather feed on it. Mosquitoes do not cause a pond to become stagnant! You always see firemen at burning buildings, but that doesn't mean they caused the fire... Traditional Western medicine teaches and practices the doctrines of French chemist Louis Pasteur (1822-1895). Pasteur's main theory is known as the Germ Theory Of Disease. It claims that fixed species of microbes from an external source invade the body and are the first cause of infectious disease. The concept of specific, unchanging types of bacteria causing specific diseases became officially accepted as the foundation of allopathic Western medicine and microbiology in late 19th century Europe. Also called monomorphism,(one-form), it was adopted by America's medical/industrial complex, which began to take shape near the turn of the century. This cartel became organized around the American Medical Association, formed by drug interests for the purpose of manipulating the legal system to destroy the homeopathic medical profession. Controlled by pharmaceutical companies, the complex has become a trillion-dollar-a-year business. It also includes many insurance companies, the Food and Drug Administration (FDA), the National Institutes of Health (NIH), the Centers for Disease Control (CDC), hospitals, and university research facilities. The microbian doctrine gave birth to the technique of vaccination that was blindly begun in 1796 by Edward Jenner. Jenner took pus from the running sores of sick cows and injected it into the blood of his "patients." Thus was born a vile practice (immunization/vaccination) whose nature has changed little to this day, and whose understanding is still clouded by Pasteur's theory. This also gave birth to the development of antibiotics, the first being penicillin in 1940. An antibiotic is the poisonous waste from one germ used in the attempt to kill another. Penicillin is the poison from a fungus. This has created the proliferation of aggressive and stubborn forms of resistant strains that haunt us today. The Rife Universal Microscope, developed in the late 1930's and early 1940's, clearly established that germs (microorganisms) are the result of disease (scavengers of dead cells) rather than the cause thereof. If germs are involved, they arise as primary symptoms of that general condition. Though germs don't cause disease, secondary symptoms are produced in response to their activity (commonly called the disease). One reason the conventional medical community doesn't see the big picture is their means of looking at it. A lot depends on how you look at it and what you look at it with. Read more:http://www.laleva.org/eng/2004/05/louis_pasteur_vs_antoine_bchamp_and_the_germ_theory_of_disease_causation_1.html